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USMLE EXAM SLIDES!!!

Tarek Hassouna
47,XYY
Paternal cause @ meiosis II
-gamete receiving both copies of
one homolog (in this case YY)

Prophase
=> crossover

4 chromosomes
2 types

2 chromosomes 1 chromosomes
2 types – All x 2 1 types – All x 4
Can not flex
elbow!

Biceps brachialis
Biceps brachi
Brachial Plexus
Cannot ABduct! arm

Deltoids

Cannot extend
wrist

Claw hand –
lesioned by tauma
to heel of hand
-fracture of hook
of hammate
Nerve innervations of arm

Dr CuMa
Radial nerve injury = wrist drop
Ulnar nerve injury = claw hand
Median nerve injury = Ape hand
The hands

Guyons Canal – associated with


ulner nerve injury!! - claw hand!!!
Anterior
Leg compartments
Deep posterior
compartment
compartment
Unhappy triad

Medial collateral ligament

Anterior cruciate ligament

Lateral Meniscus

A blow from the lateral side of the knee causes a tearing of the medial
coll lig. – occurs among foot players
This occurs because of attachment of the lateral meniscus
which tears
Medial meniscus is associated with the ACL – so that also tears
Thus, you get the unhappy triad…
Postnatal derivates
fetal remanant
Umbilical vein Ligamentum teres hepatis - falciform
ligament
Umbilical arteries Medial umbilical ligament
Ductus arteriosus Ligamentum arteriosum
Ductus venosus Ligamentum venosum
Foramen ovale Fossa ovalis
allantois Urachus – median umbilical ligament
notochord Nucleus pulpos of invertebral disc
Celiac trunk

Spleenic
Left gastric

Right gastric Common


hepatic
Hepatic proper

Gastroduodenal

Left
Right gastroepiploic
gastroepiploic
Hesselbach Triangle Direct hernia
-hasselbech triangle
-medial to epigastric artery
-external ring!!!

indirect hernia
-internal deep ring
-into the scrotum –
compresses sperm chord
-infants

Rectus abdominis muscle (medially)


Inferior epigastric vessels (superior and
laterally).
Inguinal ligament, sometimes referred to as
Poupart's ligament (inferiorly)
Contralateral Medial surface of brain
-face + arm paralysis + sensory loss -leg+ foot area
-aphasia (dominant) -sensory cortices
-left sided neglect

Contralateral
Most common site of CoW -homonymous hemianiopia with
aneurysm!! macular sparing
-visual field defects -visual changes

Locked in syndrome
- CNIII is intact

Most common site of aneurysm!! Ipsilateral


-CNIII palsy -faical paralysis
-cochlear paralysis
-Vestibular
-facial pain + temp
-dystaxia

Contralateral loss of pain + temp


Ipsilateral
-dysphagia
-hoarsness
Bilateral hemiparisis
-decreased gag reflex
Contralateral proprioception deficit
-facial pain + temp
Ipsilateral paralysis of hypoglossyl
-trigeminal nucleus
-ataxia
MoA:
Treatment /DOC:
Block the presynaptic
Neuropathic pain
reuptake of 5HT + NE +
DA
-increased levels!!!

Nortrptyiline
Desipramine
Imipramine
Clomipramine
Amitriptyline
Adverse effects!!
Things to know!!
Anticholinergic effects!!
Impramine – eneuresis
Orthostatic HypoTN
Nortryptiline – least
Dry mouth + confusion +
orthostatic!!
sedation
Clomipramine – most
serotonergic TCA!!
Cardiac tox!!
MoA:
Treatment /DOC:
Reuptake inhibitor only
DOC!! – depression
for seratonin!!!
Premature ejeculation
Bulemia
OCD
Panic disorder

Fluoxetine
Citalopram
Sertraline
Escitalopram
Paroxetine
Adverse effects!! Fluvoxamine
Things to know!!
Nausea
DOC!!
Headache
Seratonin syndrome = 2
Diahrrhea
SSRI + 1 MAO
Restlessness + insomnia
Fluoxamine – OCD!
Seratonin syndrome
MoA:
Treatment /DOC:
Block the enzyme
monoamine oxidase

Tranylcypromine
Phenelzine

Adverse effects!!
Things to know!!
Must have tyramine free
tyramine free diet!!
diet!!

HTN crisis!!
-tx with phentolamine +
nitropurriside
Calculating + interpreting Risk
Risk Equation Interpretation
Odds ratio (a/b)/(c/d) = ad/bc Odds of having disease in
exposed group vs.
unexposed
Relative Risk a/(a+b) / c/(c+d) getting the disease
exposed vs. unexposed
Attributable risk (a/a+b)/(c/c+d) Difference
Exposed vs. unexposed
Diagnostic testing
Disease (+) Disease (-)

Test (+) TP FP

Test (-) FN TN

Sen => TP/(TP+FN)


Spec => TN/(TN+FN)
SNOUT => Sensitivity rules OUT!
SPIN => specificity rules IN!
Sleep stages description EEG readings
awake Awake + alert
Active + mental
concentration - Beta waves

Awake but eyes closed -


Alpha waves

1 Light sleep

2 Deeper sleep- bruxism

3-4 Deepest non REM sleeep


Sleepwalking
Night terror
Bed wetting
REM Dreaming loss of motor
tone
erections
Tachycardia
More than 100 BPM
Atrial fibrillation
What to know:
-uncoordinated
-irregularly irregular
-upper chambers quiver –
bag of worms appearance
Atrial flutter

What to know
-coordinated electrical stimulation –
regularly irregular
- due to a loop of electricity in the upper
chambers of the heart.
Supraventricular tachycardia

What to know:
-repeated periods of very fast heartbeats begin and end
suddenly
-Same as paroxysmal SVT
Wolf-Parkinson White

What do you need to know:


- extra (accessory) connection
- most common causes of fast heart rate
disorders (tachyarrhymthmias) in infants and
children
Perfusion vs. Diffusion vs. Airway
problems
problem PaO2 PaCO2 pH RR Clincal
presentation
Restrictive – Decrease decrease increase increases SOB!!
Perfusion defect -causes pul Pul HTN
HTN!! Narrow S2
Fungus Loud S2
Protozoates RV hypertrophy
Cancer S4 sound –
Neuromuscular increases on
diseases inspiration

Inpiratory crackles
+ alveolar
infilitrates –
hyaline disease
Obstructive – Decreased Increases decrease increases Tachypnea
airway -CO2 retainer!!! SOB!!
Bacterial!! – pneumotactic
center
stimulated!!
V/q mismatch
V/Q PaO2 PaCO2
high Increased – thus perfect Decreased – since
environment of ventilated, Co2 can escape!
tuberculosis
low Decreased – no ventilation Increased – no ventilation
to that area!! to that area!!
Antiarrythmics in kids
Ventilatory and ABG patterns in Coma
Breathing Metabolic pH, PaCO2, Specific Conditions
Pattern Pattern HCO3
Hyperventilation Comp pH < 7.3 Uremia, DKA, lactic
Hypocapnia =>
Metabolic PaCO2 < 40 acidosis, acute sepsis,
vasoconstriction =>
decreased CSF formation acidosis HCO3 < 17 salicylates, methanol,
ethylene glycol
Hyperventilation Respiratory pH > 7.45 Hepatic failure, acute
Hypocapnia => alkalosis PaCO2 < 40 salicylate intoxication,
vasoconstriction =>
decreased CSF formation HCO3 > 17 pychogenic causes, sudden
onset dyspnea

Hypoventilation Respiratory pH < 7.3 Respiratory failure from


acidosis PaCO2 < 90 CNS or PNS disease, chest
HCO3 > 17 conditions or deformities

Hypoventilation Uncomp pH > 7.45 Alkali ingestion. Usually no


Metabolic PaCO2 > 45 impairment of
alkalosis HCO3 > 30 consciousness; suspect
psychogenic
Low volume state!
Toxic Syndromes
Group BP P R T MS Pupil Peris- Diaphor- Other
size talsis esis

Anticholinergic -/  ±  Delerium    Dry mucous


membranes,
agents flush, urinary
retention

Cholinergic agents ± ± -/ - Normal to ±   Salivation,


depressed lacrimation,
urination,
diarrhea,
bronchorrhea

Ethanol or sedative-    -/ Depressed ±  - Hyporeflexia


hypnotics
Opioids     Depressed   - Hyporeflexia

Sympathomimetic     Agitated  -/   Tremor, seizure


agents
Withdrawl from     Agitated,    Tremor, seizure
confused
ethanol or sedatives
Withdrawl from   - - Normal,    Vomiting,
anxious rhinorrhea,
opioids piloerection,
diarrhea

Goldfrank’s Toxicologic Emergencies, 2006


Glycogen storage diseases
Glycogen Storage disease Enzyme deficiency CP Keywords
Von Griekes Type I Glucose 6 phosphatase Hypoglycaemia Lactic acidocis
Hepatomegaly Hyperurecemia
Hyperlipidemia Protuberant belly
Failure to grow Xanothomas on buttocks

Pompe’s type II Acid maltase Hepatomegaly Death by age 2


Muscle weakness Heart failure
Tendionous Xanthomas!!
Cori’s / Forbes type III Glycogen debrancher Hypoglycaemia Glycogen debrancher!!!
Hepatomegaly Accumuation of dextrin like structures
Hyperlipidemia in cytosol
Causes myopathy -no fatty infiltration

***Anderson Type IV Glycogen brancher Hepatospleenomegaly Cirrohsis!!!


Cirrohosis
Failure to thrive

McArdles type V Muscle glycogen Excersise induced cramps Renal failure


phosphorylase  rhabdomyelosis -dark urine!!!
-myoglobinuria

Her’s Type VI Liver glycogen phosphorylase Hypoglycaemia


Hepatospleenomegaly

Taruis Type VII Muscle PFK Excersize induced cramps Growth retardation
Weakness Haemolytic anemia
Hypernatremia
Hypernatremia

Vascuar Renal Endocrine GIT

Hypovolemia Glycouria
Main cause!! – if water Diabetes insipdus Conns syndrome
Severe watery diahrrea
is down then Na+ Decreased Cushings disease
concentration rises vasopression
Hyponatremia

Hyponatremia

Renal GIT Respiratory Endocrine CNS Cardiac

Nausea
Severe diahrrea Vomitting Lidocaine toxicty –
Increased cortisol –
SIADH – increased ADH Small cell carcinoma prolonged QT interval –
Vomitting Addisons Headache Na+ channel blocker
Malaise

Concentrated urine increased H2O retained


Cerebral edema – oliguria
Hypercalcemia

Hypercalcemia

Cancer – T-cell
GIT CNS Cardiac Renal Endocrine Respiratory
leukemia

Psychotic noise Primary


Constipation - hardens Stones – calcium hyperparathyroidism Small cell carcinoma –
Depression Short QT interval
feces oxalate PTH secreted!!
Confusion Lithium use
Name of disease Genetics Enzyme deficient CP/Diagnosis/treatment Description
Fabrey’s disease X-linked recessive Alpha galactosidase A Deficiency results in the accumulation of
Angiokerotomes globotriacyl ceramide
- tiny painless papules on the body (thighs, - accumulates in blood and leads to impairment
buttocks, lower abdomen) of the blood vessel system
Vortex keratopathy
-destruction of cornea
-but this does NOT affect vision
Peripheral Neuropathy
CVD’s
Diagnosis
- fetal amniocentisis
- chorionic villus sampling
Treatment
- enzyme replacement
Goucher’s disease Autosomal recessive B-glucocerebrosidase Hepatospleenomegaly MOST common LSD!!!
Hyperspleenism - also called the “housekeeping” disease
- enhanced destruction of RBCs, WBCs, and Results in the accumulation of glycosylceremide
platelets => leads to anemia - deposits in spleen, liver, kidneys,
Cirrohsis bonemarrow and lungs
Osteoporosis - BUT, for some reason, there is no
Blood work abnormality seen in the heart, lungs, or
- increased alkaline phosphotase kidney
- increased ACE 3 types
- increased Ig levels - Type I => early life – no CNS involvement
Treatment - Type II => six months
- enzyme replacement - Type III => any age – systemic involvement
- mannose glucocerebroside
MG should be taken 60 units/kg – intravascular IV
every 2 weeks
Tay Saches Autosomal recessive Hexoamidase A Cherry red spots on macula – this is only Deficiency results in accumulation of GM2-
On chromosome 15 -def in alpha subunit suggestive!! gangliosidases
If Bsub – then Sanoff’s Optic atrophy Three types
disease Diagnosis - Type I – neonatal
- serum levels of hexoamidase should be - Type II – childhood
low - Type III – late onset
- whirling appearance in slides of tissue
- onion skin
Treatment
- substrate reductase therapy
Neimans Pick disease Autosomal recessive Sphingomyelinase Enlargement of sleep + liver Deficiency of sphingomyelin
Foamy cytoplasm
Enlarged lymph nodes
Death occurs within first year of life
Metachromatic leukodystrophy Autosomal recessive Aryl Sulfatase A Dementia Deficiency leads to accumulation of cerebroside
Ataxia sulfate
Treatment
- Bone marrow transplantation
- Stem cell transplantation
Mucopolysaccharideosis Autosomal recessive Alpha-2 iduronidase Corneal ulceration – clouding!! Deficiency results in accumulation of heparin
- Hurlers – most severe!!! Gargoylism sulfate + dermaton sulfate
Course facial features
Developmental delay
Diagnosis
- chorionic villus sampling
- amniocentisis
Treatment
- enzyme replacement
- Bone marrow transplant
- Umbilical cord transfusion
Mucopolysaccharideosis X-linked recessive Iduronate sulfatase Aggreesive “hunting” behavior Defiency leads to accumulation of leparin
- Hunters Treatment sulfate + dermaton sulfate
- enzyme replacement
Acid base disorders
pH = 6.1 log ([HCO3-]/(0.0301)PCO2
pH can be decreased by decreasing HCO3 or by increasing PCO2
pH can be increased by increasing HCO3 or by decreasing PCO2

pH HCO3 PCO2 compensation


Respiratory increased Decreased – by Decreased Renal
alkalosis compensation -increased
excretion of
HCO3
Respiratory decreased Increased – by increased Renal
acidosis compensation -increased NH4
use!
Metabolic Increased Increased Increased – by Lungs – keep CO2
alkalosis compensation – hypoventiliation

Hypokalemia
Metabolic decreased decreased decerased Lungs – eliminate
acidosis CO2 –
hyperventilation
Enzyme kinetics
competitive Non-competitive
Slope (Km/Vmax) increased increased
Y-intercept (1/Vmax) unchanged increased
X-intercept (-1/Km) increased unchanged
O2 binding curve
O2 affinity This upward spike is due
increases!! to the fact that the
combination of the first
heme in Hb and O2
increases affinity for the
second, then the third,
then the fourth!!
This occurs at 100%
saturation of O2

- When fully saturated, each


gram of Hb contains 1.39 mL
of O2

O2 affinity
deccreases!!

In any case of
chronic blood
loss – there is
less Hb
avalible!! –
function of it is
still normal!!
Valvular disorder – left side of heart!!
Murmurs

Increased Ventriclular Increased atrial pressure -


pressure - >120 mm Hg >15 mmHg

Aortic Mitral
valve valve
pathology pathology

No pressure
Pressure gradient gradient Atrial pressure
Artial pressure increase at
b/w ventricular + between vent. increase at diastole
systole
aoartic + aor.

Aortic Mitral
regurgitati stenosis Mitral
Aortic regurgitation
stenosis on

Hypervolemic/prolapsing LHF lLHF


S4 gallop pulse
LVH Opening snap Laterally displaced apex
Early diastolic murmur
Midsystolic Loud S1 Pansystolic murmur
Descendo
murmur Middiastolic Thrils towards the axilla
Best heard leaning
Thrills – radiation forward Crescendo Loud P2
to carotix Plato
Visible suprasternal
Reverse S2 split pulsations S3 gallop
Split S2
Valvular disease – right side
Murmurs

Ventricular
Atrial pressure
pressure >25
>5 mm Hg
mmHg

Pressure No pressure
Atrial pressure Artial pressure
gradient b/w gradient
increase at increase at
ventricular + between vent.
diastole systole
aortic + aor.

Pulmonary Pulmonary Tricuspid Tricuspid


stenosis regurgitation stenosis regurgitation

JVP – prominent
RHF + Pul HTN Early diastolic JVP – giant A wave Y descent
JVP – prom A wave murmur Mid-diastolic JVP – large v
Parasternal heave murmur wave
Midysystolic murmur Best heard on Parastenal heave
inspiration
Thrill – radiation to left Pansystolic
shoulder murmur
S2 split
Increased
Insulin

Liver Fat cells Muscle

Carbs Fat Protein Carbs Fat Carbs Protein

Dec. GNG
Dec. Glycogenolysis increased Decreased
breakdown Increased glucose Increased FAA Inc. glucose uptake Increased
Increased glycolysis lipogenesis
uptake syn Increased glycolysis AA uptake
Increased Increased
glycogenesis
lipolysis Increased glycerol Decreased Inc. glycogenolysis Increased
synthesis lypolysis protein
synthesis

Increases lipoprotein lipase


Hemolytic
Anemia

Glucose
Glycolysis
Uridyl transferase Galactokinase
Hexokinase ATP -> ADP + Pi Phosphogluco
+ GIT mutase
G6P Glu-1P Gal-1P Galactose

G6P Isomerase
CP: - vomiting, jaundice, hyperbilremia,
Deficiency leads to
F6P
hyperglycemia, lethargy, cirrohsis galatosemia + galatosuria
ATP -> ADP + Pi Treatment – eat/drink milk products •causes cataracts and
-ATP, Citrate, Glucogon mental retardation at young
F26-BP
PFK 1 inhibit PFK1 in high ages
PFK II amounts

F16-BP
F1P Fructose

Fructose 1P uridyl Fructokinase


Glyceraldehyde-3P transferase
Deficiency in FK
Rate limiting Enzymes!!
-fructoseuria – a hereditary condition
+ Rate limiting step in
DHAP Aldolase CP – vomiting, diahrea, apathy, liver damage leading to
Glycolysis
jaundice
Triosphosphat •if it reaches the kidney, you get Fanconi syndrome!
e Glycerol 3P •Failure of resorption of fructose
Isomerase Think of expired drugs – adverse reactions cause this
syndrome
G3P 1,3 BPG CP: hypophosphatenemia, renal glycosuria, hypourecimia
Lactate
dehydrogenase
NAD -> NADH
Lactate
23-BPG
dehydrogenase
ADP + Pi -> ATP
> NADH -> NAD +
3PG
H+
Phosphoglycerate
kinase
Deficiency is an autosomal recessive disorder
2 PG
•it affects survival of RBCs because RBCs
Phosphoglycerate
can only rely on glycolysis and nothing else
mutase
- treatment – spleenectomy and blood
transfusion PEP
Phosphoenolpyruvate
Enolase Pyruvate
+ H2O Kinase Pyruvate

ADP + Pi -> ATP


>
Alanine Deficiency of alpha 1-4
glucosidase
aminotransferase Alanine
•type II Pompes
Pyruvate •type III Cori’s
Pyruvate carboxylase •type IV Anderson’s
+ Biotin Malate
dehydrogenase
Oxaloacetate Malate

PEPkinase Basically, in order for


Glycogen
oxaloacetate to be
converted back into
Phosphoenolpyruvate glucose, you need a Glycogen
shuttle for it to go into the synthatas Debranching
e enzymes
cytoplasm
Branching Glycogen
Phosphorylase
2-PG enzymes

Deficiency results in UDP-glucose


3-PG
Type V McArdles (in
muscle) and Type VI
Her’s (in liver)
1,3-BPG Uridyl
Transferase
UTP->UDP + PI

G3P

G1P
DHAP
Review : It’s the rate limiting
enzyme!!!
•increase ATP
•increase glucogon Phosphogluco
•increase citrate Deficieny (Type 7) F16BP
Mutase +
These all inhibit the enzyme = Tori ‘s Disease PFK glycogenine

F16- F6P
BPtase
Note :
Increase in glucogon =
G6P
Inhibiting the entire glycogenisis process
Factors influencing: Insulin, G6P, excess
Deficieny (Type I) liver glucose
= Von Giekes Disease
G6Pase GLUCOSE
Cell trauma

Inhibited by Cortisol
Cell wall release
phospholipase

PLC PLA2

Lipoxygenase
20 carbon
Arachnoic acid

Inhibited by
indomethicin
HPETE (hydroperoxyeicosatetranoic
Facilitates acid)
closer of PDA Leukocyte
COX1,2 chemotaxis

Leukotriens
Inhibited by asprin
Celecoxib

Prostoglandins
Inhibition of platelet
Note: All 3 eicosinoids induce inflammation!!!
aggregation;
Redness—An insect's sting will trigger the classic inflammatory response. Short acting vasoconstrictors — TXA2—are
vasodilation;
released quickly after the injury. The site may momentarily turn pale. Then TXA 2 mediates the release of the vasodilators
PGE2 and LTB4. The blood vessels engorge and the injury reddens.
Prostacyclin
Swelling—LTB4 makes the blood vessels more permeable. Plasma leaks out into the connective tissues, and they swell.
The process also looses pro-inflammatory cytokines – C5a + bacterial products Stimulation of platelet
aggregation;
Pain—The cytokines increase COX-2 activity. This elevates levels of PGE2, sensitizing pain neurons. vasoconstriction

Heat—PGE2 is also a potent pyretic agent. Aspirin and NSAIDS—drugs that block the COX pathways and stop prostanoid Thromboxane
synthesis—limit fever or the heat of localized inflammation.
Beta Oxidation
Source ATP Total
1 FADH2 X 2 ATP 2 ATP
1 NADH X 3 ATP 2 ATP
1 acetyl CoA X 12 ATP 12 ATP
Total 17 ATP

C(2n)
(n-1) 14 + 10 -2 = total ATP
Ex. Palmitate - 16 carbons – C2(8) - n=8
8-1 x 14 + 10 – 2 = 106 ATP
Source ATP Total
7 FADH2 x 2 ATP = 14 ATP
7 NADH x 3 ATP = 21 ATP
8 acetyl CoA x 12 ATP = 96 ATP
Activation = -2 ATP
NET = 129 AT
Apoproteins
Apoprotein Function Deficiency
Apo B APOB "unlocks" the doors High levels =>
to cells and thereby atherosclerosis + heart
delivers cholesterol to disease
tissues
Low levels => fat mal
From Intestine to tissue absorption - because fat
cannot be transported!
Apo B100 => VLDL
Apo B48 => chylomicrons
Apo A Aka HDL - the good Low levels =>
cholesterol ! atherosclerosis
Apo C Activates lipoprotein Low levels – impairs
lipase- degrades lipoprotein lipase
chylomicrons -heparin injection test

Abdominal pain =>


pancreatitis
Apo E Allows for liver for triglyceride and cholesterol
chylomicrons + IDL to be levels in blood if deficient
taken in by liver
Glomerular filtration rate
Afferent Efferent

Assessing Assessing
-RBF -RPF
-GFR -PAH
-Creatinine
Prerenal pathologies – results in afferent constriction!!! -BUN
-decreased RBF
-Inulin
-decreased GFR
-increased Creatinine in plasma!!! – why? Because bowmens oncotic pressure is decreased – thus, “sucking power” is decreased!!!

In response
-renin -> ang II constricts efferent arterioles
-decreased RPF
-decreased PAH
-decreased BUN in blood

BUT then...turns into renal!!!


Normally
Kidney function Normally
-AngII constricts
-PGE dilates efferent
afferent -increased GFR
-increased GFR -decreased RPF
-increased RPF
This increase FF!
NSAIDS INHIBIT
THIS!!! ACE inhibitors
inhibits this!!! –
nephrotoxic!!
Inulin PAH
-freely filtered -free filtered
-not secreted -free secreted
-not reabsorbed -not reabsorbed
-freely exrected -freely excreted
Parameter Equation Key words

clearance Renal Equations


Cx = Ux (Vx/Px) If decreased – mostly reabsorbed

if increased– mostly secreted


Glomerular filtration rate GFR = Ui (Vi/Pi) = Ci

Starling forces GFR = Kf[(Hgc – Hbs) – (Ogc – Obs)] Increased Hbs = >obstructive
nephropathy

Decreased Hgs = hypotension

Increased Obs = minimal change disease

Decreased Ogc = hypoalbuminea


Renal plasma flow Upah x V/Ppah Decreased PAH clearance => efferently
arterial secretion
Filtration fraction FF = GFR/RPF Decreased RPF = increased AngII -
inhibted by ACE

Increased RPF = increased prostaglandins


– inhibited by NSAIDS
Water clearance Ch20 = V - Cosm With ADH => CH2O is greater than 0

Without ADH => CH2O is less than 0


Filtered load GFR X Px GFR = Ui (Vi/Pi) = Ci

GFR = exretion rate / Pi = Ci

Excretion rate V X Ux
Left ventricle assessment
Aortic regurgitation– Soft S2

Aortic stenosis– Loud S2

Mitral stenosis – Loud S1

Mitral regurgitation– soft S1


Prerenal vs. Renal
problem Etiology Initially after BUN /Cr ratio

Prerenal Renal artery stenosis Afferent AngII restablishes GFR! >20


CHF Decreased GFR
Low volume state! Decreased RBF Afferent
Increased serum Cr Increased GFR
Decreased RBF
Efferent decreased serum Cr
Decreased RPF
Increased serum BUN Efferent
Decreased RPF
Increased serum BUN

Renal glomerulonephritis, acute Afferent AngII restablishes GFR! <20


tubular necrosis Decreased GFR
acute interstitial nephritis Increased serum Cr Afferent
Vancomycin tox!! Decreased GFR
Efferent Increased serum Cr
increased RPF
Decreased serum BUN Efferent
Decreased RPF
Increased serum BUN
Post renal Urinary tract obstruction
BPH
Kidney stones
Nephrotic syndrome
Suspect kidney
disease

Nephrotic
syndrome

Proteinuria - >3.5 g/day


Hypoalbuminea
Edema
Hyperlipideamia

Non-
Proliferative
proliferative

Mesangial Endocapillary Membranoprolif Minimal Focal Membranous


proliferative prlif change segmental

Immune
Lupus + IgA Parvo B- Tram-tracking Diffuse loss of Only some complex in BM!
nephro 19 appearance podocyte foot glomeruli + only
part of it! Spike + dome
Immune complex in processes =>
mesangium!! fusion!! Subepithelial
Nephritic syndrome Nephritic
syndrome

Proteinuria – under 3.5 g/day


Hematuria
Azostomia
RBC casts
Oliguria – less than 400 mL/day

Type II Type III


Type I rapidly rapidly rapidly
progressive progressive progressive

Type Type
II HS II HS Wegners
Microscopic
granulomato
polyangitis
sis
Goodpasture Post Diffuse IgA
s strep proliferative GN nephro/berge
rs C-ANCA
Linear IF - antiBM Lumpy-
bumpy Wiring loop Saddle nose pANCA
Poor prognosis Subendothelial deformitiy
Subepithelial IC deposits in
Hemoptyisis + Ics – C3 Anti-DNA Ics in mesagnium Pulmonary
oliguria mesagnium infections
Children
URTI Ass. With anti-
Acute gastritis neutrophil
antibodies
Obstructive vs. restrictive
parameter Obstructive Restrictive
Lung capacity Increased OR normal decreased
Residual volume increased Decreased
FEV decreased Decreased
FEV/FVC decreased increased
80% gone? <80% >80%
Cardio equations
Parameter Equation Key points

Compliance increase in blood volume in a vessel when


the pressure in that vessel is increased

Thus, if pressure increases, compliance


decreases => hypertension!!!
Resistance Adenosine => decreased resistance!!!

Cardiac Output CO = SV x HR During exercise


-increased SV
CO = rate of O2 consumption/(arterial O2 -increased CO
content – venous O2 content)
Prolonged excerise
-increased CO
-increased HR – if too high => decreased CO
=> V-tachy
Mean arterial pressure =CO x TPR So if pressure increases, so does CO!
=2/3 diastolic pressure + 1/3 systolic MAP = SV x HR x TPR
pressure -if CO increases, so does SV, HR

Or Also
MAP = (EDV-ESV) x CO x HR
-the more EDV, the more stroke volume
-the more ESV, the less stroke volume

TPR = MAP/CO
Thus, if you increase TPR, you decrease
CO!!

Preload = ventricular EDV Increase preload with:


-blood transfusion
-excersise
-excitement – sympathetic

Decrease preload by
-venocilators - NO

Afterload =MAP If you increase MAP, you increase after load


proportional to peripheral resistance BUT if I decrease it, with hydralazine =>
decreased afterload!!

Ejection fraction =(EDV-ESV) / EDV Normally 55%


-measuring ventricular contractility – so how
much blood is ejected from the ventricle
Input
-HCO3 Output
-NH4+ -Urea!!!

Urea cycle

Deficiences + disease

Key enzymes X-linked Deficiency of this causes


hyperammonemia
Carbamoyal phosphate CP:
synthase Lethargy
-regulated by N-acetyl Hyperventilation
glutamate Vommiting + Seizurues + Hepatomegaly
Coma -> Death

Increased orotic acid production => def of


ornithine transcarboxylase
Deficiences + disease

Deficiency of Phenylalanine hydroxylase leads to PKU –


Output its an acquired disorder!!

Tyrosine -CP:
Dopamine During birth, child is normal
if its untreated child may develop
Catecholamines mental retardation
loss of motor control
Melalin
Input autistic symptoms
pale skin
Phenylalanine white blond hair
microcephaly
increased levels of phenylalanine
decreased social interaction
verbal/non-verbal communication problems
obsession
mousy odour!!!
Phenyl alanine Treatment – semisynthetic diet with reduced
phenylalanine
but because its essential, patient should take small
quantities
Aspartame – nutrasweet – should be completely
restricted from diet for life!!
Key enzymes Women who do not take enough Phe during pregnancy
have a high risk of having a child with
- microcephaly
- mental retardation of child
Phenylalanine hydroxylase -low birth weight
HG oxidase
Deficiency of HG oxidase leads to Alcaptonuria
its results from the accumulation of HG
increased excretion of HG
if patients urine is exposed to air, it turns dark colored

CP: Ochrosis
its an autosomal recessive disorder
results in pigmentation and calcification of bones and
cartlidge – leads to arthritis
Output
Seratonin
Melatonin
Nicotinate
Input
trytophan

Tryptophan

Deficiences + disease
Key enzymes
Hartnups disease!!
None we need to know
-defect in the reabsorption of the
AAs in the kidney – one of them is
tryptophan!!
-Pellegra like sympotomes
Diarhhea
Depression
Dermatitis
Sometimes cerebellar ataxia
Tryptophan
Output
HMG CoA
Acetyl CoA +
Propionyl CoA
Deficiences + disease
Input
BCAs Maple syrup urine disease
lethargy, dehydration, and vomiting
-hypotonia
BCAs -dramatic weight loss
-ketoacidosis (if untreated)- eventually leads to
Key enzymes coma and death

There are 5 types:


2-ketoacid dehydrogenase -classical MSUD *** MOST SEVERE
complex of enzymes -Intermediate MSUD
-Thiamine responsive MSUD
-Enzyme responsive MSUD w/ lactic acidosis

Propanoic acidemia
-deficeny in propionyl CoA carboxylase = met.
Acidosis, dehydrtation
-accumulation of propanoic acid
-drives formation of acetyl CoA to the formation of
ketone bodies
BSA disease hypoglycemia Ketoacidosis
MUSD increased Increased
Propanoic acidosis increased Increased more!
-drives formation of ketone
bodies form acetyl CoA
Methylmalonyl CoA Increased more! Increased more!
acidosis -accumulated
-inhibition of pyruvate methylmalonic + propanoic
carboxylase + acids
gluconeogenesis by
methylmalonyl CoA
Genetics USMLE problem
Population

Carriers Affected Children

Find p Find ratio of


Find q Find F(aa) = q^2 affected vs. Non-
Find F(Aa) = 2pq affected

If both conditions If either one


Subtract patient +
– multiply with condition, add
subtract diseased
carrier prob with carrier prob
Genetic diseases
Disease

Autosom
Autosom X-linked
al X-linked
al dominan
Dominan recessive
recessive t
t

Trinucleotid Vitamin D resistant


Cancer Collagen Lesch – Nyhan
Metabolic e repeats rickets
syndrome
disorders + Retinobalstoma
steroid Ehler-Danlos Hunters + Fabreys
– Rb gene
synthesis G6PD
Li – Fraumani = Osteogenisis
Hemoglobin Spinocerebellar p53 imperfecta Hemophilias
ADA defient ataxia Most
FAP = APC
SCID Huntingtons immunodeficiences
disease HNPCC = PMS,
Complement MSH, MLH Fragile X + Rett
deficiencies Myotonic syndrome
dystrophy Breast cancer =
Cystic fibrosis BRAC1 Duchenne + Beckers
Muscular dystrophy
Renal clear cell
= VHL

Increased paternal age


=> achondroplasia
Increased maternal age
=> Downs syndrome
Autosomal dominant diseases
Autosomal dominant disease Chromosome/gene KW

achondroplasia FGF recptor 3 Head and trunk are normal size


Advanced paternal age
AD polycystic kidney disease Chr. 16 Always bilateral
APKD1 Berry aneurysms
Infantile form is recessive
Familial adenomatous polyposis Chr. 5 More than 100 polyps!!- 100%
APC carcinoma
Familial hypercholesteremia – type II A LDL receptor Tendonous xanthomas => achillis tendon

Hereditary hemorrhagic telangectasia ? Ass. With atriovenous malformations

Herediatry spherocytosis Spectrin Hemolytic anemia


ankyrin Increased MCHC
Huntingtons disease Chr. 4 Decreased levels of GABA + Ach
Trinucleotide CAG repeats
Marfans syndrome fibrillin Subluxation of lenses
Dissecting aortic aneurysms
Floppy mitral valve
MENs Ret gene => type IIA + IIB Type I => zollinger syndrome - PTH
stimualtes histamine release
Type Iia => pheo + medullary CA +
parathyroid hypoplasia
Type IIIa => pheo + med CA + mucosal
neuromas
Neurofib type I Chr 17 Café au lait spots
Linch nodules
Neural tumors
Neurofib type II Chr 22 Bilateral Acoustic neuromas
NF#
Tuberous sclerosis Incomplete penetrance Ash leaf spots
Variable presentation
Von hipple-Lindau VHL gene Hemangioblastomas of retina,
Chr. 3 cerebellum,
Bilateral renal cell carcinoma
Lab technique – strep vs. staph
Bacteria

Catalase Catalase (-
(+) )

Coagulase Coagulase
Hemolysis
(+) (-)

Staph Aureus
Novobiocin Novobioci
-yellow + beta hemolytic Alpha Gamma Beta
(+) n (-)
-Mannitol (+)
DNAse (+) Optichin
(+) Optichin (-) Bile Bacteraci Bacteraci
6.5% NaCl Staph Staph
epidermis Bile salt Bile salt (-) Esculin (+) n sen n res
saprophyticus
is (+)
-others!! Group A S.
Strep Strep
6.5% (+) 6.5%(-) Strep. Aglatactai
pneumonia viridins
Pyogenes e

Group D
Entercoccus
S. Bovis
Capsulated bacteria
Organisms
Strep pneumonia
Klebsiella pneumonia
Bacillus anthracis
Haemophilus influenza B
Pseudomonos Aerug
Neisseria meningitis
Cryptococcus neoformans
Common causes of meningitis
Newborn (0-6 Children (6 months 6 – 60 years 60+
months) – 6 years)
Group B strep S. pneumonia S. pneumonia S. pneumonia

E. Coli N. Meningitis N. Meningitis N. Meningitis

Listeria H. Influenza Enterovirus Listeria


Viral Protein synthesis
(+) RNA RNA dep RNA Pol

Translation

(-) RNA Reverse transcriptaise

RNA dep RNA Pol How retroviruses


(HIV) does it!

RNA cDNA DNA-dep DNA Pol

Reverse Transcriptase mRNA

DNA mRNA

DNA dep RNA Rol (host) Structural proteins


Gene Proteins Function
Env HIV virus
GP160
GP120
GP120 – mediates CD4 +
chemokine co-receptor
Gp41 binding
GP41 – mediates fusion
Gag P17 P17 – matrix proteins that
P24 stabilizes envelope
P7.9 P24 – capsid – used for
serology!!
P7.9 – nucleocapsid associated
with RNA
pol Reverse transcriptase RT – produces dsDNA provirus
Integrase Int – proviral dsDNA
Protease integration into host cell
Protease – cleaves
polyproteins during assembly
process
TAT Transcriptional activator Upregulates transcription
REV Regulator of virion protein Viral replication
expression
NEF Regulatory factor Negative regulator factor
Virus reviews – key USMLE ones!!!
Virus Lab Keywords

Parvo B19 ssDNA – smallest!! Kids – rash – slab of cheek!! – red + blotchy!!
Naked Fetal hydrops fetalis!!!+ acute polyartrhitis
Ico
Measles - Rubeola ssRNA (-) Koplick spots!!!
Enveloped Rash – red+flat+slightly bumpy – spreads
Helical down from head to shoulders
Segmented!!
Polio ssRNA Paralysis + gastroenteritis
Naked
Acid resistant!
Divides in enucleated cells!!!
HPV 16 +18 Naked Cancer in sexually active smoker
dsDNA
Ico
Mumps ssRNA (-) Parotitis
Enveloped Orchitis
Helical Make infertility
Segmented!!
Rubella ssRNA (+) Cataracts leading to blindness in newborns
Enveloped PDA!!
Ico
Varicella zoster dsDNA Vesicular lesions in dermatomal pattern
Naked
Tegemented!!
Tzmack smear!!- see Cowdry type cells!!
CMV dsDNA Acute retinitis in AIDS patients
Naked
Tegemented!!
HPV 6+11 Naken Gentical warts
dsDNA
Ico
Circular!!!
PAP smear
Koilocytic atypia!!
HSV 2 dsDNA Painful genital vesicular lesions
Naked
Tegemented!!
Hep E ssRNA Fever
Naked Abdominal pain
Vomitting
Diahrrea
High mortality in pregnant women
Rabies ssRNA (-) Encephilitis following animal bite –
Enveloped intracellular negri bodies in neurons
Helical
Bullet shaped!!
EBV dsDNA Teen with fatigue spleenomegaly, atypical
Naked lymphocytosis, (+) heterophil Ab test
Tegemented!!
-t8-t14
Norwalk Gastroenteritis on cruise ship

Coronavirus ssRNA (+) Runny nose


Enveloped -common cold
Helical
RSV ssRNA (-) Rapid shallow breathing = brochiolitis!!
Enveloped
Helical
Segmented!!
Hanta ssRNA (+/-) – only ambisense!!! Hantavirus – pulmonary edema- fever,
Enveloped muscle, aches, increased WBC, low platelet
Helical counts - ARDS
Fungus Lab Keywords

Pneymocystis jiroveci Silver stain (+) HIV patient – CD4 count <200
Bactrim (-)
“Hat-shaped cyst
Candida albicans Germinal tubing!!! Thrush = cancer patient on chemo
Culture - budding yeast + septated
In you – pseudohyphae
Crypto. neoformans Visualize with india ink!! HIV = meningitis!!
Capsular antigens in CSF – latex
agglutination
Urease (+)!!
Histoplasma capsulatum Oval yeast cells Lung granulomas - Ohio river valley
Septated hyphae Intracellular yeast!!
Tuberculated macroconidia Macroconidia
urine antigen
Microsporium Ringworm!! Tinea curis, capitis and pedis
-Trichosporon beigelii – hair shafts!! Wood lamp visualization!
-Trichophyton mentagrophytes – scalp
-
Coccidiodomycosis Spherule w/ endospores Lung granulomas – San Joaquin valley

Aspergillus True hyphae!!! Fungus ball in lung!!


-septated with branches – acute angles -angioinvasive
45 degees
Blastomycosis Broad based budding yeast!! Systemic mycosis
-lungs + bone + skin
Microconidia
Sporothrix Cigerette shaped!! Ascending lymphadenitis
Resembles a daisy flower Rose gardening!!!
Mucormycosis Non-septated!! Rhinocerebral infection
90 degree branching!! Diabetic ketoacidosis
Malaria treatment
Plasmodium Primaquine Chloroquine Quinine Mefloquine
Vivax Yes – in the NO Pregnancy Prophylaxis – if
liver Pregnancy res to chloro
Ovale Yes – in the NO – resistant Pregnancy Yes – if
liver Pregnancy resistant to
chloro
Malarae NO Yes + prima Preganancy Prophylaxis – if
Pregnancy res to chloro

Falciparum NO NO IV – if cerebral Prophylaxis – if


pregnancy + pregnancy res to chloro
Teratogenic Drugs
Drugs Effects

ACE inhibitors nephrotoxic

Alcohol Fetal alcohol syndrome


Mental retardation
Alkylating agents - anticancer drugs!! Absence of digits
-cisplatin
-cyclophosphamide
-procarbazine
Aminoglycosides CN VIII toxicity = > ototoxicity
-streptomycin nephrotoxicity
-neomycin
-gentamycin
cocaine Fetal addition
Fetal development
Placental abruption
Diethylstilbestrol Vaginal clear cell adenocarcinoma

Folate antagonists Neural tube defects


-methotrexate
-sulfamethoxazole + trimethaprim
Iodide Hypothyroidism - congential goiter
Lithium Ebstiens anomaly
-atrialized right ventricle
Maternal diabetes Caudal regression syndrome – anal atresia
RDS?
Smoking (nictotine, CO) Preterm labor + placental prolems IUGR, ADHD

Tetracyclines Yellow teeth

thalidomide Limb defects

valproate Inhibition of intestinal folate absorption

Vitamin A excess High risk for spontaneous abortion + birth defects + cardiac
abnormalities
Warfarin Bone defects
Fetal hemorrhage
abortion
Anticonvulsants Spina bidfida
-carbamazepine
P450 inhibitors
Drug indication Often combined with to become toxic

ritonavir Protease inhibitors for HIV infection NNRTI


indinavir efavirenz
nelfinavir nevirapine
Etravirine
=>become toxic ! -
erythromycin Macrolides – 50S inhibitor Sivastatin
telithromycin preventing the transfer of the tRNA bound Ergot drugs - migraine
clarithromycin at the A site of the rRNA complex to the P Verapamil
site of the rRNA complex
fluconazole Anti-fungal agents Warfrin
ketoconazole
Itraconazole
Verapamil – works on heart!! Ca2+ channel blocker Warfrin
-arrythmia + HTN Ergots
-varient angina - vasospastic PPIs
zoplicone
Chloremphenical 50S inhibitor Not really used drug
preventing the transfer of the tRNA bound -cuases grey baby syndrome
at the A site of the rRNA complex to the P
site of the rRNA complex – prevents peptide
bond formation
Cimitidine H2 receptor blocker PPI
-GERD + peptic ulcers Opiods
-Zollinger Ellison Chemotherapy – dox + etop + vin blast +
vincris
Amiodareone Antiarrythmic Class III– K+ and Beta blocking Warfrin
action Sildenafil
Procainamide
Digoxen
cyclosporine
P450 inducers
Drug indications Will inactivate the
following drugs
phenytoin Anticonvulsants BDZ
carbamazepine Sex hormone agonists +
oxcarbazepine antagonists
SSRIs
Phenobarbitol For Fibrile seizures!!! BDZ
efavirenz NNRTIs for HIV PI’s
nevirapine
etravirine
rifampin Tb infection
St.Johns Wort Major depression
Grisofulvin Antifungal/bacterial
pioglitazone Oral hypoglycemic
-peroxisome proliferator-
activated receptors
Epileptic drugs
Drug MoA First line for
Phenytoin Na+ blocker Partial
tonic-clonic
Carbamazepine Na + blocker Tonic –clonic
-results in decreases SHFRF Trigeminal neuralgia
Valproate Type T Ca2+ blocker Myoclonic
-inhibits GABA transaminase – BUT – can be used for
increases [GABA]!! treatment for ALL types of
sieuzures
Phenobarbital Increases action of GABA-A Febrile seizures
-They also block glutamate
receptor excitation
High dose – blocks K+ + Na+
channels
Diazepam + lorazepam Facilitates actions of GABA For acute status epilepticus
-results in hyperpolarization of
the membrane
Platelet vs. Coagulation

Bleeding disorder

Platele Coagulati
Mixed
t on
Lab Hemo Von
Factor Hemop Vit. K
- inc. bleeding philia Willibr DIC
VII def hilia A def
time B and
Decrease
-decreased Factor Factor
Increased BT d PC,
platelet count Increased PT Factor IX II, VII,
everythin
VIII IX, X Normal or
Glanzman Normal PT Normal g else
Bernar Soulier Idiopathic TP Thromb Increased increased increased
n Normal PT
otic TP PT PTT !!!
PT Increas
Normal PC
Decreased Decreased PC Increase ed PTT Increased
Increased Decrease PTT
PC Increased BT d PC d PTT
BT
Increased BT Megakaryotcyt Increased
Decreased
Decreased GpIIb/IIIa es BT
GpIb Anti-GpIIb/IIIa Pentade!!

Ristocetin test!
Make slide on thalassemia

gene desc anemia

-a/aa Single gene absent Silent carrier

-a/-a Two genes absent Mild anmeima

--/aa Two genes absent Mild anemia – but more fatal for next
generations -> death inutero

--/-a HbM Moderate anemia

--/-- HbBart present – all 4 genes absent Severe anemia


Respiratory curves

Obstructive Restrictive Mixed


-COPD, asthma -pulmonary fibrosis Emphysema!!
-Pneumoconisosi -centri = smoking
-ALL neurmuscular -pan = a1at def
disease!!!
Coombs test
Coombs test

Direct Indirect

RBCs with IgG Combines with Combines with


antibodies rabbit anti-IgG Add test blood O rabbit anti-IgG
RBCs to test tube
of IgG antibodies

If agglutinates =>
If agglutinates =>
erythroblastosis
Hemolytic anemia
fetalis
Different types of immunity
Immunity

Active Passive

Natural Artificial Natural Artificial

give antigen Antibody is give immune


antigen enter + given
body makes serum – or the
the antibody is
made antibody Life- Mom to fetus - actually
long IgA antibody
immunity!!!! antivenom
Ex. Polio
vaccine- life-
long!!
HS type
Type I
Source
Hypersensitivity reactions
IgE-mediated
mediators
Basophils
Discription
Initiall exposure
Clinicals
Anaphylaxis
Mast cells -body sees antigen -> B-cells ->
Histamine increase in plasma cells -> antibodies
Bradykinin from IgE
IgE 2nd exposure
TNF -ab is already formed
IFN gamma -it binds to mast cells + basophils
PLA2 First get degranulation
-primary mediators – heparain,
histamine, proteases
-cytokines – TNF, IFN gamme, IL-1
-phospholipase A2 – prostaglandins +
LTB4
Type II Complement MAC complex Comp dep ADCC
dependent C3a + b - opsinin -Lysis – Ag+Ab -> stimulates Parasitic infection
ADCC C5a complement system + disrupts Tumors
Ab mediated cellular membrane integrity by forming pores Type II diabetes M – juvenille!
dysfunction -Opsinins – fixed complement coats Pernicious anemia
Antigen with Ab – enhances Cellular dysfunction
phagocytosis Mysinia Gravis – DDx- lambert eaton –
defect in release of Ach from neuron
ADCC Graves disease
-IgG coats -> non-sensitized cells Wegner’s granulomatosis
destroy -antibodies against proteinase 3 – patch
-for worms and tumors necrosis of BVs
-facilitate the killing of insulin- P.ANCA – Ab against myeloperoxidase
producing cells Pemphigus – Ab attack desmosomes –
Ab mediated lung hemorhages
-Ab against surface receptor + Complement dependent
changing their function -transfusion
-erythroblastosis fetalis
-autoimmune haemolytic anema
Type III Ag+ Ab complex Complement Induced by Ag/Ab complex that Generalized – serum sickness
proteins produced tissue damage!!! – - Amyloidosis
IgG + IgM because they activate complexes - sarcoidosis
-circulating complexes -> Local – arthrus reaction
produces damage because they - bacterial – actinomycets –
deposit at sites of tissues => causes lung + brain abcess
attract neutrophils + acute transplant rejection
macrophages
-in-situ complexes – attach to FC
receptor on polymorphs – release
cytokines attract PMN + initiate
MORE complex - > more
complement fixation!!
1st stage – formation of Ag/Ab
complex
2nd stage – deposited complexes
in tissue
3rd stage – inflammatory
reaction!!
Type IV Cell mediated CD4- TH-cells - Characterized as granulomatous Poison ivy – contact dermatitis
TNF inflammation – chronic! Tuberculin sensitivity
IFN gamma Histoplasmosis
IL-1 Sacrcoidosis
macrophages MS
Wound healing

characteristic 1st intention 2nd Intention

Duration Faster Longer

Pattern More planned – surgery injury More chaotic – crush injury

contracture Less - More contracture

Fibroblast activity Less - Fibroblast activity is more

Susceptibility to infection Less - More susceptible to infection

Surface Can be replaced Surface is defective

Inenstiy Less - more intense

Granulation Less - Larger amount of granulation

Scar Small scar - Larger scar is formed


Weird syndromes
Disease Neuro BV Renal Skin
Von Hipple Lindau Retina Capillary hemangiomas Cystic renal that could
Cerebellar complicate to Renal cell
carcinoma

Von reckling Houson PNS tumors Pigmentation of iris


-chr. 17 Optic nerve gliomas Cafe au lait spots

NF type II Acoustic neuromas


-chr. 22 meningiomas

Sturge Weber Mental retardation Facial V1 + V2 of trigeminal


Seizures Leptomeningeal
Hemiplegia

Osler Weber Telengectasia


Epstaxis
GI bleeds

Tubulosclerosis seizures Cutaneous angiofibromas Renal cysts Ash leaf spots


Liver cysts
Pancreatic cysts
Penile soars
Penile Soars

Painful Painless

Treponium – Syphilis –
HSV-2 Hemophilus Ducreyi Chlamydia
1st degree

Fever L1-L3 – painful


lymphadenopathy
Headache Inguinal
lymphadenopatthy
Painless chancre -ABC – african,
Myalgia
blindness, chronic
Vesicular!! infection
Alveolar pressure vs. Intrapleural
pressure
Conditions Transpulmonary Alveolar pressure Pleural pressure
pressure
Physiological Always (+)!!! + during inspiration (-) 5
(-) During expiration
Pneumothorax 0 +1 +1

Transpulmonary = alveolar
– pleural
1) Any lung volume - transpulmonary pressure is equal
to and opposite to elastic recoil pressure of the lung
-thus, if elastic recoil pressure is (+) on exhalation, TP is
(-)

2) Inhalation – lung volume pressure (inhalation) < lung


volume pressure (exhalation)
Exhalation – lung volume pressure (inhalation) > lung
volume pressure (exhalation)
SA node graph

Digoxin
-directin inhibtions of
Na/K ATPase =
increased Ca2+ inside
cells – increases
Esmolol- Class II contractility
-decrease Ca2+ currents
-decreases slope of
phase 4
-increases PR interval
Adrenal physiology
Cholesterol

17
Pregnolone 17 OH preg Dehydroepialdosterone

Progesterone 17 17-OH
Androstenodione
Progesterone

21 21
11 – DOC 11 Deoxycortisol Testosterone

11 11
Corticosterone Cortisol DHT

18 17 OH def => Hypertenion, decreased androgen


synthesis
Aldosterone
21 OH def => Hypotension, increased androgen
synthesis
11 Oh def => Hypertension, increased androgen
synthesis
Adult Diahrrea Excessive infusion
Normal
Whole blood loss of normal saline

Diuretics Edema SIADH


Addisons RHF
Inc. H2O
21-OH deficiency Cirrhosis
Nephrotic syndrome consumption

Osmotic diuresis Diabetic Insipidus Antibiotics


Sweating Fever Inc. HCO3
[Drug] plasma vs. Time
measurement Drug X Drug Y
Vd decreased increased
Cl decreased increased

Drug X
[drug] Cl = rate of elim / [drug]
plasma Vd = rate of elim/ [drug]Ke

Drug Y

Time
Prader Willi vs. Angelman
Maternal Paternal
Deleted Imprinted Deleted Imprinted
Prader Willi Yes Yes
-Chr. 15
Angelman Yes Yes
-Angelman
Galactose metabolism?
Enzyme Clinical presentation Accumulation
Galactokinase K for cataracts!!! Galactol
-galactosemia
-no smile
Uridyl transferase Jaudice Galactol
Hepatomegaly
Mental retardation
B-galactosidase Abdominal distention UDP galatose
Diahrrea
ANP production
Hypertension

ANP release in
response to
increased pressure

Atria Ventricles

Due to LV
Increased blood
hypertrophy due to
volume?
HTN

Kidney
-decreased
reabsorption of
Na+ H2O
Lab values – Renal
parameter Normal Value
BUN 10-20
Cr 1
Na+ 135-145
Cl- 98-108
K+ 3.5 – 5.5
HCO3 24
PCO2 40
P02 60-90
Glucose 70-100
P-Osm 300
U-Osm 350-450
P- 2-4
Mg 2-4
Ca2+ 8.8-10.8
Luman PCT(85%) Plasma

Na + Cl- -> NaCl + 2K+ Clinicals


PO4 3- -Alkalosis => low volume
Na + Fanconi protein state
-Dehydration => increased Na
Ca 2+
resorption + increased HCO3
Mg 2+ + AA + Glu
Acetazolamide -> induces RTA
H+ II
-treatment for increased ICP
HCO3
CA
H2O +CO2 H2O + CO2 Fanconi syndrome +
Tetracycline => low energy
CA state => S3 + cardiomegaly

H+
HCO3
HCO3
Loop of Henle – ascending
Luman Plasma
Cl- What to know:

Na 1) Decreased urine Osm –


diluting portion -
K
2) Furosemide, Toresemide,
Mg Butemide, Ethrynic acid
Ca 3) Barters syndrome!! – defective
Na+/K+ ATPase – thus –
hypomagnesmia +
hypocalcemia

Gymnastics + Aneorexia + Bulemia


DCT late
Lumen Plasma

K+

Aldosterone
Na+
Clinical notes
-Thiazides that act here
cause hypokalemia
How? – Low volume
state – response is to PTH
increase aldosterone – Vit.D Ca2+
results in hypokalemia! ATPase
K+/H+ exchange
HCO3!!!!
-collecting duct – plasma
-major source of
to cells
bicarbonate absorption

Collecting ducts!!!

Urea cycle
Glutamine -> NH4 +
-NH3
Glutamate

Glutamate -> alpha KG +


NH3

80% of H+ comes from


here
Asprin OD

Increased absorption
of ASA
Early • Mixed acidosis => you
are ingesting more acid
• Respiratory alkalosis and retaining more CO2

Later
• ASA gets absorbed
• Results in met. Acidosis +
Resp. Alk
• pH is NORMAL!!!
Renal tubular acidosis
RTA Urine pH K+ Notes
I increased decreased Stones!! Ca2+
Disfunctional K+/H+
channel
@collecting duct
II Decreased decreased PCT
Dec. HCO3
resorption
III Normal decreased Inherited
Carbanhydrase
deficiency
IV decreased increased Decreased
aldosterone
response
Collecting ducts
Lumen Plasma

Na+
Na+/K+ exchange Clinical
K+ -increased aldosterone =>
Alkalosis – thus,
spirolactone can induce
acidosis!!!

K+
Aldosterone
H+
Vagnial bleeding
Woman

Vaginal
Bleeding?

Placenta abrupta Endometrial Ectopic


Hydaform mole
– if pregnant carcinoma pregnancy

Increased Beta
Painless!!! Postmenapausal Pain!!
HCG
Dexamethasone suppression test
Give Dex

Low dose

Still
Decreased
increased
cortisol
cortisol

Healthy!! High dose

Decreased Increased
cortisol cortisol

Pituitary Increased Decreased


Cushings ACTH ACTH

Small cell Tumor of the


carcinoma adrenal
Inhalation vs. Exhalation
TP AP IP

Inhalation More (-) 0 to -1 to 0 -5 to -8

Exhalation Less (-) 0 to +1 -8 to -5


-due to elastic
recoil
Joint pathology
Joint
pain?

Erosive Non-erosive

1 joint Multiple joints SLE


Fibromyalgia
Asym Asym Sym

Gout Reiters B-19 infection


pseudogout Lyme Rheumatic
disease fever
Rheumatoid
arthritis –
hours!
Osteoarthritis -
<30 mins +
distal joints
Platelet vs. Coagulation
Bernard Soulier Glanzmann ITP TTP
PT – normal PT – normal PT – normal PT – normal
PTT – normal PTT – normal PTT – normal PTT – normal
PC – decreased PC – normal PC – decreased PC – decreased
BT – increased BT – decreased BT – increased BT – increased
KW: KW: KW: KW:
GpIb GpIIb/IIIa Megakaryotcytes! Pentade! – fever
adhesion No clumping! HUS

Hemophilia – factor VWF DIC Vit K. Def


VIII PT – normal PT – increased PT – increased
PT – normal PTT – normal OR PTT – increased PTT – increased
PTT – increased increased PC – decreased PC – normal
PC – normal PC – normal BT – increased BT – increased
BT – increased BT – increased KW KW
KW: KW: -trauma + spesis -general
-Xlinked recessive AD -shistocytes -protein S + C
-hemarthrosis Ristocretin test! -fibrin split products
MI evolution
0-4 Minimal change -> reprofusion injury
4-12 hrs Edema + hemorrhage
12 hrs – 1 day Coagulation necrosis
1 to 5 days neurtophils
5-10 days macrophages
10-14 days Granulmoas + neovascularization
2 weeks to 2 months Scar formation
Increased in: POS!!!
-endometrial carcinoma –
GnRH hormones
adenosquamous CA –
MC!! GnRH
-CP – postmens bleeding
-papillary adeno – mets to
lungs

-
Increased in:
FSH
LH -ectopic pregnancy
-hyditaform mole
Parital = 69XXX
Complete – syn + cyto

androgens

aromatase Ovaries

estrogen Progesterone Beta-HCG


Motor CNs
Efferent

General Special

Visceral Somatic Visceral Somatic

Sweat Tongue
Saliva Muscle of eye Mastication
NONE!
Gut Muscles of tonge Swallowing
Pupil contriction Facial muscles
Sensory neurons
Afferent

General Special

Visceral Somatic Visceral Somatic

Palate
Vision
Carotid Pain + temp in face + Taste
Hearing
Sinus ears smell
Equilibrium
tongue
Heart murmurs
Valve Systole Diastole (early) Diastole (late)

Pulmonary + Aortic Middle Pulmonary Aortic reguritation


Stenosis regurgitation
-left shoulder =>
pulmonary
-Apex to carotid =>
Aoartic

Tricuspid + mitral Holo/Pan Tricuspid stenosis Mitral stenosis


=> Reguritation
Normocytic
anemia

Non-haemolytic Hemolytic

ACD
Aplastic anemia Intravascular Extravascular
Kidney disease

Intrinsic extrinsic Intrinsic Extrinsic

PNH Autoimmune cold Spherocytosis DIC


Mechanical G6PD TTP
trauma PK def HUS
Aortic stenosis Sickle Cell Infection
Prostethic valve HbC defect Methyl DOPA
Autoimmune - Penicillin
warm
S2 Split (reverse)
-Boom Baroom
LBBB
Aortic stenosis S3 sound (Bell)
IHSS Boom – Ba – Boom –
increased elastic limit
CHF
Mitral regurgitation
Dilated cardiomyopathy

S4 sound
-Bell apex – gallop
“Baboom-Boom”
-non-compliant ventricle
Aortic stenosis + LVH

S1 Split
-Baroom Boom
RBBB
If you hear... Then its Due to: KWs
Holosystolic Mitral regurg Ischemic heart disease Squatting on hand
blowing Tricupsid regurg Mitral valve prolapse grip!!!
VSD LV dilation – dilated Kids!
cardiomyopathy

Midsystolic Aortic stenosis Age related calcification calcification


Ejection Bicuspid aortic valve
murmur
Midsystolic Mitral valve Marfance sydrome Squatting on hand
Click prolapse Ass. With infective grip!!!
endocarditis
Rheumatic fever
Blowing Aortic Rheumatic fever
High pitched regurgitation Syphalis!!
diastolic
Opening snap Mitral stenosis 2ndary rheumatic fever
Rumbling – buttonhole – fish
mouth
Machinary like PDA child
murmur