Course Instructors: Dr. Francis, Dr. Wolf and Dr.

Bautista
Hemostasis
Lymphoma & Leukemia
251
Amino Acids
Biochemistry
Endocrinology
Neurophysiology
Hematology
Vitamins, Minerals, Trace Elements
Cellular Physiology
Membrane Physiology
244
Low Energy State
Inflamation
Nephritic-Nephrotic
254
248
218
Reproductive Endocrinology
Renal Physiology
76
159
171
192
220
Gastrointestinal Physiology (GI) 135
5
45
53
55
80
87
64
71
105
116
125

Electrolyte Physiology
Pulmonary Physiology
Neuromuscular Physiology
Vascular Physiology
Cardiac Physiology
Page Lecture
Note Pages
Welcome to the Program
Rheumatology
238
PASS PROGRAM
USMLE REVIEW STEPS 1, 2 AND 3
Course Instructors: Dr. Francis, Dr. Wolfe & Dr. Bautista
184
1
Anabolic Pathways
Cancers
Immunodeficiencies
Lymphocytes
Leukocytes
Immunology
Catabolic Pathways
Protein Structure and Function
Enzymes
Microbiology
Antibiotics
Granulocytes
Biochemistry, Glycolysis,
Gluconeogenesis & TCA
Viruses
497
515
Antibiotics (Dr. Cordova)
Surgery & Trauma (Dr. Cordova)
413
453
477

408
292
303
329
335
344
371
262
277
282
351
358
369
Obstectrics and Gynecology
Note Pages
The Four Hypersensitivities 366
2
PASS PROGRAM
USMLE REVIEW STEPS 1, 2 and 3
Week 1 Monday Tuesday Wednesday Thursday Friday
Introduction Behavioral science Test taking/Time mgt. Membrane Phys Cardio Patho
logy
7:15-9:009:00 am Low Energy State EKG Phys Cardiac Phys 7:15 am Low Energy State
EKG Phys Cardiac Phys
1 hr break Vitamins Psychiatry Arrhythmias Murmurs
10:00-12:00 Minerals Endocrine Phys
Trace elements Endo Path
LUNCH
1:30-4:00pm Cellular Phys Psych Endo Neuromuscular Cardio
Vascular Phys
Week 2 Monday Tuesday Wednesday Thursday Friday
Gastrointestinal Surgery Principals Pulmonary phys Renal Phys Neuro Phys
7:15-9:00 Physiology
1 hr break Trauma Pulm Path Renal Path Neuro Path
10:00-12:00 GI Path
LUNCH LUNCH
1:30-4:00pm
GI Ansthesia Pulm Renal Neurology
Week 3 Monday Tuesday Wednesday Thursday Friday
Amino Acids OB Glycolysis Ketogenesis Nucleotides
7:15-9:00 Protein structure Gluconeogenesis GlycogenGlycogen 7:15 9:00 Protein s
tructure Gluconeogenesis
1 hr break Protein function GYN Fructose/Galactose Pentose Pathway
10:00-12:00 OB/GYN Pharm Pyruvate metab.
LUNCH
1:30-4:00 pm Quaternary protein Reproductive TCA cycle Amino acids DNA
Repro Pharm Lipolysis Fatty acid synth.

Week 4 Monday Tuesday Wednesday Thursday Friday

Oncology Pediatricts Leukocytosis Rheumatology Myobacteria, Spiro.
7:15-9:00 Development Leukemia's Rickettsia
1 hr break Myelodysplasia Normal Flora Virus
10:00-12:00 Pediatricts Pharm Gram+/LUNCH
Oncology l Immunology l Granulocytes l t Fungus O I G F
1:30-4:00pm Imm. Deficiency Hypersensitivities Parasites Closing remarks!!!
Transplantation Protozoa
Dr. Francis
CellularCellular physiology
Dr. Wolf
TimeTime management
Teaching Associates
Antibiotics-Antibiotics Dr Cordova (datee TBA) physiology
Behavioral
Cardiology
Pulmonary
Biochemistry
Reproductive
Immunology
Pediatricts
Oncology
management
Endocrine
Rheumatology
Gastrointestinal
Renal
Neurology
Microbiology/Antibiotics
OB/GYN
Dr Cordova (dat TBA)
Surgery/Ansthesia- Dr Cordova
Hematology- Dr Qi (date TBA)
Statistics- Dr Qi (date TBA)
DNA/RNA- Dr Bautista
Biochem pathways- Dr Lee
3
4
5 5
6 6
7 7
8 8

9 9
10 10
11 11
12 12
13 13
14 14
15 15
16 16
17 17
18 18
19 19
20 20
21 21
22 22
23 23
24 24
25 25
26 26
27 27
28 28
29 29
30 30
31 31
32 32
33 33
34 34
35 35
36 36
37 37
38 38

39 39
40 40
41 41
42 42
43 43
44 44
4/30/2008
1
Making the most
out of your time
here at the PASS
program !!!
Making the most
out of your time
here at the PASS
program !!!
Study smart
not hard
Study smart
not hard
Power is in
knowledgegegg !
Power is in
knowled !
NBME-NBME- National Board
of Medical Examiners
National Board
of Medical Examiners
For For
profit
company
NBME-NBME- National Board
of Medical Examiners
National Board
of Medical Examiners
Shortage of family
doctors throughout
US
Shortage of OB/GYN
physicianshysicians in Fl,
Shortage of family
doctors throughout
US

 Shortage of OB/GYN
p in Fl, py
Texas, California, and
Michigan
Cutoff for USMLE
Steps were raised
from 182 to 185?
py
Texas, California, and
Michigan
Cutoff for USMLE
Steps were raised
from 182 to 185?
Youre the next cutting edge
physician
20,000 new residents
Your pay?ay?
Youre the next cutting edge
physician
20,000 new residents
Your p
What do you want to do when
you finish medical school?
What do you want to do when
you finish medical school?
py
Radiology, Dermatology,
Ortho.
Those making decisions,,
control how many come
across the bridgeridge
py
Radiology, Dermatology,
Ortho.
Those making decisions
control how many come
across the b
45
4/30/2008
2
Why do so many fail the
test?
Why do so many fail the
test?
ZOO

THEORY THEORY
A physician sits and writes a question based
offf of the disciplineiscipline theyy wantt to testst you on
A hhologistshologists l i t dss thee titiontion thee
A physician sits and writes a question based
of of the d the wan to te you on
A h l i t d th ti th
How do they comprise a test
that is written for you to fail?
How do they comprise a test
that is written for you to fail?
A psyc rewordd th ques th way
your mind thinks
This is why the wrong answers always look
good
A psyc rewor th ques th way
your mind thinks
This is why the wrong answers always look
good
5 PASS rules in answering
question
5 PASS rules in answering
question
1. Cover the answers
2. Read the lastast sentence and decidede iff
it is a clue or concept
1. Cover the answers
2. Read the l sentence and deci i
it is a clue or concept
5 PASS rules in answering
question
5 PASS rules in answering
question
1. Cover thehe answers
2. Read thehe last sentenceence and decideide if it is
a clue or concept question
1. Cover t answers
2. Read t last sent and dec if it is
a clue or concept question
it is a clue or concept
question
3. Read the vignette, and isolate the
facts of the vignette
4. Compriseprise a thought process
5. Look down, click and move !!!!!!!
it is a clue or concept

question
3. Read the vignette, and isolate the
facts of the vignette
4. Com a thought process
5. Look down, click and move !!!!!!!
3. Readad the vignette,ignette, andd isolateolate the factsacts
of the vignetteignette
4. Comprise a thought process
5. Look down, click and move !!!!!!!
3. Re the v an is the f
of the v
4. Comprise a thought process
5. Look down, click and move !!!!!!!
A 38 y/o woman has congestive heart failure,
premature ventricular contractions and
repeated episodes of ventricular tachycardia.
Her blood pressure is normal and there are no
murmurs. Her heart is markedly enlarged.
A 38 y/o woman has congestive heart failure,
premature ventricular contractions and
repeated episodes of ventricular tachycardia.
Her blood pressure is normal and there are no
murmurs. Her heart is markedly enlarged.
Coronaryy angiographygiography shows no abnormalities.ities.
Whichh of the followingollowing is the
most likelyly diagnosisgnosis ?
Coronar an shows no abnormal
Whic of the f is the
most like dia ?
A.Acute rheumatic fever
B.Congenital fibroelastosis
C.Constrictive pericarditis
D.Myocardial infarction
A.Acute rheumatic fever
B.Congenital fibroelastosis
C.Constrictive pericarditis
D.Myocardial infarction
E.Primary cardiomyopathy E.Primary cardiomyopathy
A.Acute rheumatic fever
B.Congenital fibroelastosis
C.Constrictive pericarditis
D.Myocardial infarction
A.Acute rheumatic fever
B.Congenital fibroelastosis
C.Constrictive pericarditis
D.Myocardial infarction
E.Primary cardiomyopathy E.Primary cardiomyopathy
46

4/30/2008
3
USMLE Step 2 and Step 3 approach USMLE Step 2 and Step 3 approach
Whathat is the next best step in management?
Is the patientnt stable?table? (basedbased on hemodynamics)modynamics)
-Unstable:nstable: ABCsBCs
- Stable:: readead the vignetteignette
W is the next best step in management?
Is the patie s ( on he
-U A
- Stable r the v
Do you have enough information to make a
definitive diagnosis?
-Yes- treat
- No- order a test (BLIS)
blood/labs/image/surgery
Do you have enough information to make a
definitive diagnosis?
-Yes- treat
- No- order a test (BLIS)
blood/labs/image/surgery
A 23 y/o man who is HIV positive has a 2 week
history of midsternal chest pain that is aggravated
by eating spicy foods; the pain is unrelated to
exertion or position and he reports no dysphagia.
Treatment with H2 receptor blocking agents has
provided no relief. He takes clotrimazole for
thrush and zidovudine (AZT).AZT).)) He has a CD4+ T
A 23 y/o man who is HIV positive has a 2 week
history of midsternal chest pain that is aggravated
by eating spicy foods; the pain is unrelated to
exertion or position and he reports no dysphagia.
Treatment with H2 receptor blocking agents has
provided no relief. He takes clotrimazole for
thrush and zidovudine ( He has a CD4+ T (
lymphocytecyte count of 220/mm3mm3 (N>500).).
Which of the following is the most
appropriateopriate next stepep inn
management?gement?
(
lympho count of 220/ (N>500
Which of the following is the most
appr next st i
mana
A.Therapeutic trial of acyclovir
B.24 Hour pH probe

C.Acid perfusion test

D.Esophageal manometry
A.Therapeutic trial of acyclovir
B.24 Hour pH probe
C.Acid perfusion test
D.Esophageal manometry
E.Esophagoscopy E.Esophagoscopy
A.Therapeutic trial of acyclovir
B.24 Hour pH probe
C.Acid perfusion test
D.Esophageal manometry
A.Therapeutic trial of acyclovir
B.24 Hour pH probe
C.Acid perfusion test
D.Esophageal manometry
E.Esophagoscopy E.Esophagoscopy
Procrastination in doing
questions
Procrastination in doing
questions
How many read before doing
questions?
Whatat t testingesting ti ?
How many read before doing
questions?
Wh t t ti ? Wh are you t ?
2 weeks later, what
happens?
Wh are you t ?
2 weeks later, what
happens?
Procrastination in doing questions Procrastination in doing questions
How many read all the choices
in the explanation?
futureuture
How many read all the choices
in the explanation?
f Prior exposure to f
questions
I have a lot of
details in my head
Prior exposure to f
questions
I have a lot of
details in my head
47

4/30/2008
4
Procrastination in doing
questions
Procrastination in doing
questions
How many do the questions
in tutor mode?
How many do the questions
in tutor mode?
Driving a car
and lost
Driving a car
and lost
Its ok to be wrong !!!! Its ok to be wrong !!!!
Block of 50 question and get
45/50 correct, are you any more
prepared for the boards from the
moment you started that test?
Block of 50 question and get
45/50 correct, are you any more
prepared for the boards from the
moment you started that test?
If you get 30 /50 wrong, you will
not be very happy
Found a hole, that can be fixed
Remember every time you fall
If you get 30 /50 wrong, you will
not be very happy
Found a hole, that can be fixed
Remember every time you fall
Why do we not listen to our first
thought?
Why do we not listen to our first
thought?
We are scared of being wrong We are scared of being wrong
We do
average
We do
average

not want our over all

to be lower than the meanean
not want our over all
to be lower than the m

My friends told me to do as
many questions as I can
before I take the test

My friends told me to do as
many questions as I can
before I take the test
6000 questions
Multiple banks
You are doing questions to learn
from them
Do we order test to learn about a
pathology
(i.e. Hypothyroidism TSH panel)
6000 questions
Multiple banks
You are doing questions to learn
from them
Do we order test to learn about a
pathology
(i.e. Hypothyroidism TSH panel)
3 steps to studying::
1. Obtain the information
2. Questions
3. Results of the bank
3 steps to studying
1. Obtain the information
2. Questions
3. Results of the bank
Questions: Organ system based
50 question
Questions: Organ system based
50 question
Do they ask youou 50 new things?
Pathologicalogical presentation doesoes not
change, just the story lineine (cluesues are
so important)
Willill youou see the pattern in mixed
blocks?ocks?
Do they ask y 50 new things?
Pathol presentation d not
change, just the story l (cl are
so important)
W y see the pattern in mixed
bl
What bank to use? What bank to use?
Q-BankQ-Bank USMLEUSMLE Rx. USMLEworldUSMLEworld Rx.
Do you see a pattern?
At the end of your first week,
you will be evaluated by several

tutors to determine which is the

best test bank for you to use.
Do you see a pattern?
At the end of your first week,
you will be evaluated by several
tutors to determine which is the
best test bank for you to use.
48
4/30/2008
5
What should I
results of my
What should I
results of my

do, with
question
do, with
question

the
bank?
the
bank?

50 questionsuestions completed
(what is right or wrong)
Example: Polyhydramnios:ramnios:ramnios:ramnios: Downownwnwn syndromeyndromendro
mendrome
50 q completed
(what is right or wrong)
Example: Polyhyd D s Example: Polyhyd Do sy
What is the mostst commonmmon cardiac
abnormality?
Write the subject matter
Look for patterns in the question
This is what you will read about
Example: Polyhyd Do sy
What is the mo co cardiac
abnormality?
Write the subject matter
Look for patterns in the question
This is what you will read about
What do most students do What do most students do
Vignette..gnette.. Downs syndromee
Answer: Endocardialal cushionon defect
Read about it from the author
Transcriberanscribeee to noteoteee cardsdsss onn ECDCD
Vi Downs syndrom
Answer: Endocardi cushi defect
Read about it from the author
T to n car o E Transcrib to not card on ECD
Readad the notesotes about ECD

 Read the CMDT about ECD

Harrisons and read about ECD
Are you any more prepared for
Downs syndrome on thehe boards?oards?
Transcrib to not card on ECD
Re the n about ECD
Read the CMDT about ECD
Harrisons and read about ECD
Are you any more prepared for
Downs syndrome on t b
NBME practice exam NBME practice exam
On line at http://www.NBME.org
Step 1 5 forms (do not take form 3)
Step 2 3 forms

On line at
Step 1 5
Step 2 3
Step 3 1

http://www.NBME.org
forms (do not take form 3)
forms
form

When should I take

may NBME ?
Step 3 1 form
When should I take
may NBME ?
Not enough time in the day !!!!!!!
- Exercise
- 210 score
- Proper sleep hygiene - Proper sleep hygiene
-Take time out to
reward yourself
PASS program clues vs. class notes PASS program clues vs. class notes
You should drill the PP-clues with a
partner for at least 1 hour a night.
( hour new, hour random review)
You should drill the PP-clues with a
partner for at least 1 hour a night.
( hour new, hour random review)

Caution
Teacher
Caution
Teacher

inn drillinglling classass notes:

vs. Student
i dri cl notes:
vs. Student

Tutoring:: Tutoring
This is your time to ask questions that
you may have with the material
Doo questionstionstionstions with your tutor (rememberremember

 This is your time to ask questions that

you may have with the material
D ques with your tutor ( Do ques with your tutor (remember
its ok to be wrong)ong)
Yourr tutortor is there to help
you find and fix your weaknesss
Do ques with your tutor (remember
its ok to be wr
You tu is there to help
you find and fix your weaknes
49
4/30/2008
6
Tutoring cont. Tutoring cont.
Try several tutors to find the chemistry that
works for you
If you can not make it to your secession,, please
inform your tutor, so theyey can fill the spot with
another studentdent
Try several tutors to find the chemistry that
works for you
If you can not make it to your secession please
inform your tutor, so th can fill the spot with
another stu
Once you are comfortable with a
couple of tutors, there is a request
book in the back.
(The key word, just a request book)
Once you are comfortable with a
couple of tutors, there is a request
book in the back.
(The key word, just a request book)
50
Physiology:
Weeks One & Two
51 51
52 52
1

INTRODUCTION: THE MOST

POWERFUL CONCEPT IN
MEDICINE
THE LOW ENERGY STATE
WHO USES ENERGY?

BRAIN
MUSCLES
PRIMARY ACTIVE TRANSPORT
HEART
MEMBRANE MOVEMENT

RAPIDLY DIVIDING CELLS

SKIN
HAIR
GI
RESPIRATORY
RENAL(PCT)
BLADDER
ENDOMETRIUM
ENDOTHELIUM
BREASTS
SPERM
GERM CELLS
CUTICLES
BONE MARROW
RED BLOOD CELLS
WHITE BLOOD CELLS
PLATELETS
PRESENTATION OF A DISEASE
When it bothers the patient enough, he or
she will see the doctor as soon as possible
Weakness so that the patient can not go to
work
Shortness of breath scares people; they think
they might die
SIGNS OF DISEASE: WHAT YOU
CAN SEE
TACHYPNEA and DYSPNEA
SYMPTOMS: THE PATIENTS
COMPLAINTS
WEAKNESS
SHORTNESS OF BREATH
MOST COMMON INFECTIONS
PULMONARY INFECTIONS
URINARY TRACT INFECTIONS
53 53
2
OTHER COMPLICATIONS

Dry skin
Hair dry and brittle
Nails brittle
Bone marrow suppressed
Anemia
Leukopenia
Thrombocytopenia
COMPLICATIONS, cont
Endothelium atrophic
Endometrium
atrophic
Breasts atrophic
Sperm count low
GI nausea, vomiting
and diarrhea
Renal- PCT shuts
down
Bladder atrophic;
leads to UTIs
Respiratory weak
cough > infections
Germ cells unable to
replicate > leads to
skin and GI cancers
CNS: MR (children)
and dementia (adults)
CV heart failure
MOST COMMON CAUSE OF DEATH?
HEART FAILURE!!!
ANYTIME YOU CAN CONNECT TO THE LOW
ENERGY STATE
APPLY THE ENTIRE CONCEPT
THIS ACCOUNTS FOR
APPROXIMATELY 98% OF ILLNESSES
WHENEVER IN DOUBT > ASSUME IT IS
A LOW ENERGY STATE
STOP GUESSING!!!
54 54
VITAMINS, MINERALS and
TRACE ELEMENTS
THE BEGINNING
Vitamin A
A cofactor for PTH
Necessary for CSF production
Used for epithelial maturation, especially
hair, skin, and eyes
Most unique function is night vision
A mild antioxidant

Vitamin A deficiency

Poor night vision

Decreased CSF production: asymptomatic
Hypoparathyroidism
Epithelial cells fail to mature

Vitamin A excess
Pseudotumor cerebri: excess CSF
production
Hyperparathyroidism: moans, groans,bones
and stones
Pseudotumor Cerebri
Sign: papilledema
Symptom: headache
Evaluation: CT scan ( shows enlarged
ventricles)
Treatment: d/c vitamin A; serial LPs (30cc at a
time)
Main complication: blindness
This is the only cause of increased ICP where
you dont have to worry about herniation
Vitamin B1: Thiamine

Necessary for four important enzymes:

Pyruvate dehydrogenase
Alpha-ketogluterate dehydrogenase
Branched chain amino acid dehydrogenase
Transketolase

55 55
Thiamine Deficiency
Beriberi
Dry beriberi
Wet beriberi
Wernickes Encephalopathy
Receptive aphasia
Wernicke-Korsakoff syndrome
Mamillary bodies now also involved
Confabulation
Inability to move short-term memory to long-term
memory
Vitamin B2: Riboflavin
Used in cofactors ( FAD)
Best source is milk
Sunlight breaks riboflavin down
Riboflavin deficiency
Angular Cheilosis

Vitamin B3: Niacin

Necessary for cofactors ( NAD, NADH,
NADP, NADPH)
Needed by pyruvate dehydrogenase,
alpha-ketogluterate dehydrogenase, and
branched chain amino acid
dehydrogenase
Niacin deficiency
Pallegra : 4 Ds diarrhea, dermatitis,
dimentia and death
Hatnups disease: presents just like pallegra
Defective renal transport of tryptophan
Vitamin B4: Lipoic acid
Needed by pyruvate dehydrogenase,
alpha-ketogluterate dehydrogenase, and
branched chain amino acid
dehydrogenase
No deficiency state
56 56
Vitamin B5: Panthotenic Acid
Needed by pyruvate dehydrogenase,
dehydrogenase, alpha-ketogluterate
dehydrogenase, and branched chain
amino acid dehydrogenase
No deficiency state
Vitamin B6: Pyridoxine
Needed by all transaminases
INH pulls pyridoxine out of the body
Forms the cofactor pyridoxalphosphate
Pyridoxine deficiency
neuropathy
Vitamin B9: Folate
The first vitamin to run out whenever you
have rapidly dividing cells
Used to make tetrahydrofolate (THF) from
which you make nucleotides
Folate deficiency

Megaloblastic anemia
Hypersegmented neutrophils
Neural tube defects in fetuses
Mcc: overcooked vegetables

Vitamin B12: Cyanocobalamin

Needed by two enzymes:
Homocysteine methyltransferase
Methylmalonyl-CoA mutase
Used to make tetrahydrofolate
Used to recycle odd-numbered carbon
fatty acids
57 57
Vitamin B12 deficiency
Megaloblastic anemia
Hypersegmented neutrophils
Neuropathy, especially involving the dorsal
column pathways and corticospinal tracts
Mcc: pernicious anemia (type A gastritis)
Vitamin C
Used for hydroxylation
Hydroxylates proline and lysine in collagen
and elastin
Main antioxidant in the GI system
Vitamin C deficiency
Scurvy
Bleeding from hair follicles and gums
Vitamin D
Necessary for bone and teeth formation
Stimulates osteoblastic activity
Stimulates calcium AND phosphorous
absorption and reabsorption
Mineralizes bones and teeth
Vitamin D deficiency
Rickets: in children
Lateral bowing of the legs
Osteomalacia: in adults
Vitamin D resistant rickets
Defective renal reabsorption of phosphorous
As phosphorous leaks out, it pulls calcium
with it
Vitamin E
The main antioxidant in your blood
Absorbs free radicals
58 58
Diseases involving oxidation

Cancer
Alzheimers disease
Coronary artery disease
Hemolytic anemia ( esp. G6PD)

Antioxidants

Vitamin E: in blood
Vitamin C: in GI tract
Vitamin A
Beta-Carotene

Biotin
Necessary for carboxylation
Biotin deficiency
Many carboxylases would lose their
function
Vitamin K
Needed for gamma-carboxylation
Adds a third (gamma) carboxyl group to
the vitamin k dependent clotting factors
Clotting factors II, VII, IX, X, Protein C &
Protein S
Protein C has shortest half life, followed by
factor VII
Warfarin

Competitive inhibitor of vitamin K

Given orally
Always give heparin first
Crosses the placenta
Teratogenic
Follow PT ( prothrombin time )
INR 2 to 3x normal

59 59
Heparin
Acts as a cofactor for antithrombin III
Blocks thrombin, as well as clotting factors
IX, X, XI, and XII
Follow by measuring PTT ( INR 2 3X NL)
To reverse the action: protamine sulphate
If patient acutely bleeding: give FFP to
reverse immediately
What are germs good for?
Vitamins related to gut flora
They make: 90% of vitamin K
Biotin
Folate

 Panthotenic acid
They help absorb
Vitamin B12
MINERALS
Minerals
Calcium
Magnesium
Zinc
Copper
Iron
Calcium
Intracellular calcium needed for all muscle
contraction
Smooth muscle uses extracellular calcium
for second messenger systems
Atrium is ONLY membrane that uses
calcium to depolarize
Cardiac ventricle depends on extracellular
calcium to trigger off its intracellular
calcium release
60 60
Calcium, cont
Used for axonal transport
Presynaptic influx of calcium necessary for
release of ALL neurotransmitters
Needed for normal bone and teeth
development
Magnesium
A cofactor for ALL kinases
A cofactor for PTH
Interacts with potassium as well, but
location currently unknown
Zinc
Needed by hair, skin, sperm and taste
buds
Zinc deficiency: dysguisia
Copper
Needed by lysine hydroxylase in the
formation of collagen
Also needed by complex IV of electron
transport system
Copper excess
Wilsons disease
Autosomal recessive

 Ceruloplasmin deficiency
Copper deposition in lenticular nucleus (basal
ganglia), iris (Kayser-Fleischer rings) and in
the liver (causing cirrhosis)
Tx: penicillamine
Movement disorder in a middleaged person
HUNTINGTONS
DISEASE (90%)
Autosomal dominant
Trinucleotide repeats
Involves caudate
nucleus
Has anticipation
Treat with
antipsychotics
Mcc of death: suicide
WILSONS DISEASE
Autosomal recessive
Ceruloplasmin def
Copper deposition in
lenticular nucleus, liver
and iris
Treat: penicillamine
61 61
Trinucleotide repeats

Huntingtons disease
Fragile X
Fredriecks ataxia
Prader Willi syndrome
Myotonic dystrophy

Iron
Needed for formation of heme and
hemoglobin
Ferrous iron binds oxygen
Needed by complex III and IV of electron
transport system
And finally the trace elements Trace Elements
Chromium
Selenium
Molebdenum
Manganese
Tin
Flouride
Chromium
Enhances insulin action
Def: causes diabetes
Selenium

 Needed primarily by the heart

Excess: breath smells like garlic ( arsenic
as well)
Def: dilated cardiomyopathy
62 62
Molebdenum and Manganese
Needed by many enzymes in glycolysis
Xanthine oxidase: needs both elements
Tin
Needed for hair growth
Flouride
Needed for teeth and bone growth
Excess: blocks enolase of glycolysis THE END
BUT, it is really the beginning
63 63
CELLULAR PHYSIOLOGY
CELL ORGANELLS
IRREVERSIBLE CELLULAR INJURY
APOPTOSIS
CELL MEMBRANE
DISSOLVES FIRST
PROGRAMMED CELL
DEATH
NONINFLAMMATORY
PYKNOSIS
KARYORHEXXIS
KARYOLYSIS
NECROSIS
NUCLEUS
DISSOLVES FIRST
UNEXPECTED
INVOLVES
INFLAMMATION
PYKNOSIS
KARYORHEXXIS
KARYOLYSIS
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS

FAT
HEMORRHAGIC
LIQUEFACTIVE
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
64 64
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS

FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
NECROSIS
ISCHEMIC (COAGULATIVE)
PURULENT
GRANULOMATOUS
FIBRINOUS
CASEOUS
FAT
HEMORRHAGIC
LIQUEFACTIVE
MESS WITH THE
CHROMOSOMES
MONOSOMIES: DIE! DIE! DIE!
MCC: NONDISJUNCTION
90% IN DAD, USUALLY IN MEIOSIS 1; BUT
SPERM DIE ON A DAILY BASIS
FEWER OCCUR IN MOM; BUT MOM KEEPS
HER EGGS FOR LIFE AND IS THEREFORE
MORE LIKELY TO TRANSMIT HERS
IF ONE WERE TO SURVIVE TO BE BORN, IN
THE LEAST, THINGS WILL NOT GROW
65 65
TURNER SYNDROME

WEBBED NECK
CYSTIC HYGROMA
GONADAL STREAKS
SHIELD-SHAPED CHEST
COARCTATION OF AORTA

TRISOMIES
DIE! DIE!
FEW LIVE
TRISOMIE 13: PATAU SYNDROME
POLYDACTYLY
PALATE IS HIGH-ARCHED
PEE-ING SYSTEM ABNORMALITY
TRISOMIES
TRISOMIE 18: EDWARDS SYNDROME
ROCKERBOTTOM FEET (IN 95%)
TRISOMIES
TRISOMIE 21: DOWNS SYNDROME
MCC: NONDISJUNCTION
ROBERTSONIAN TRANSLOCATION:
HIGHEST INCIDENCE (33% OF
OFFSPRING)
HAS MANY THINGS TO CONSIDER

DOWNS SYNDROME
MENTAL RETARDATION 100%
IQ: AVERAGE IS 85 TO 100 WITH A STANDARD
DEVIATION OF 15
SUPERIOR INTELLIGENCE: IQ > 130
MILD MR: IQ < 70
MODERATE MR: IQ < 55
SEVERE MR: IQ < 40
PROFOUND MR: IQ < 25 NEEDS 24HR CARE
MILD TO MODERATE MR CAN BE TAUGHT BASIC
ADLS
66 66
DOWNS SYNDROME
EARLY-ONSET ALZHEIMER DISEASE
HIGHER FREQUENCY OF AML;BUT ALL IS THE
MOST COMMON LEUKEMIA
20 TO 40% HAVE congenital heart
DISEASE
-ENDOCARDIAL CUSHION DEFECTS
VSD and ASD
VSD
ASD
DOWNS SYNDROME
CYANOTIC CONGENITAL HEART
DISEASE
TRANSPOSITION OF GREAT ARTERIES
TETROLOGY OF FALOT
DOWNS SYNDROME
50% HAVE HYPOTHYROIDISM
WIDELY-PACED CRANIAL SUTURES
MACROGLOSSIA
DUODENAL ATRESIA
HIRSCHSPRUNGS DISEASE
CLUES:
MONGLIAN SLANT TO EYES
WIDELY SPACED FIRST AND SECOND TOES
SIMIAN CREASE
TRISOMIES
XXX: Normal female; has two barr bodies
XXY: Klinefelters syndrome. Tall male
with gynecomastia, small penis and
testicles
X- Fragile X syndrome
Mcc of chromosomal induced MR
Short stature; macrochordism
Collagen disorder (increased risk of MVP)
Isolated using the drug METHOTREXATE
Chemotherapy

67 67
CHEMOTHERAPY

Stops rapidly dividing cells

Attacks the nucleus in some way
Causes irreversible cellular death
WILL kill some patients
No such thing as safe chemo

ANTIMETABOLITES
ARA-A
ARA-C
5-FU: blocks thymidylate synthetase
6-MERCAPTOPURINE: promotes gout; recognized by
xanthine oxidase
THIOGUANINE
METHOTREXATE: inhibits dihydrofolate reductase(as
does TRIMETHOPRIM and PYREMETHAMINE)
Most commonly used antimetabolite
Used to treat molar pregnancies
Used to treat STEROID RESISTANT disease( followed by
AZOTHIOPRINE and CYCLOSPORINE)
ANTIMETABOLITES
METHOTREXATE
Causes folate deficiency and megaloblastic
anemia
Give LEUCOVORIN > FOLINIC ACID to
prevent the anemia
ANTIMETABOLITES
AZOTHIOPRINE
Used for steroid resistant diseases( behind
METHOTREXATE and before
CYCLOSPORINE)
ALKYLATING AGENTS
Bind to double stranded DNA
Used primarily for slow growing cancers
Cause the most nausea and vomiting
ONDANSETRON: serotonin blocker used to treat
nausea and vomiting in chemotherapy
ALKYLATING AGENTS
Bleomycin
Busulphan
Adriamycin
Cisplatnin
Cyclophosphamide
Isophosphamide
Mitomycin
Antimycin
Acridine dyes

Hydroxyurea
Melphalan
Mechlorethamine
Procarbazine
Dacarbazine
Chlorambucil

FOR RESCUES
Desroxzasane
Mesna
68 68
MICROTUBULE INHIBITORS
Vinblastine
Vincristine
Paclitaxel
NUTRIENT DEPLETION
L-ASPARAGINASE
IMMUNEMODULATORS
LEVAMISOLE
IRREVERSIBLE CELLULAR
DEATH
NUCLEAR DAMAGE
LYSOSOMAL DAMAGE
MITOCHONDRIAL DAMAGE
OCCURS IN 6 HOURS in all tissues
69 69
IRREVERSIBLE CELLULAR
DEATH
NUCLEAR DAMAGE
LYSOSOMAL DAMAGE
MITOCHONDRIAL DAMAGE
OCCURS IN 6 HOURS in all tissues
except the brain
IRREVERSIBLE CELLULAR
DEATH
OCCURS IN 20 MINUTES IN THE BRAIN
The End?
To Be Continued
70 70
MEMBRANE PHYSIOLOGY

A MEMBRANES JOB IS NEVER

DONE
WHAT A MEMBRANE DOES
PROVIDE SHAPE
AMPHIPATHIC
HYDROPHILIC and HYDROPHOBIC
WATER SOLUBLE and FAT SOLUBLE
HYDROPHOBIC wants to be INSIDE away from
water
HYDROPHILIC wants to be OUTSIDE in contact
with water
FAT SOLUBLE COMPOUNDS
DO NOT interact with the outer cell
membrane. They go right through and
head for the nucleus
HAVE NUCLEAR MEMBRANE
RECEPTORS
Concentration gradient is only limiting
factor
STEROID HORMONES
MADE FROM CHOLESTEROL
FAT SOLUBLE( hydrophobic)
Do NOT interact with cell membrane
ALL have a nuclear membrane receptor
except CORTISOL
CORTISOL has a cytoplasmic receptor;
but it still translocates to the nuclear
membrane
71 71
WATER SOLUBLE HORMONES
HYDROPHILIC
CAN NOT simply go through a fat soluble
membrane
Must bind to the outside membrane to a
receptor
Requires a SECOND MESSENGER
But first, what about ANY water soluble
compound?
WATER SOLUBLE COMPOUNDS
Factors affecting diffusion
CONCENTRATION GRADIENT
SIZE of molecule
Net charge on molecule
pH (affects the net charge of a molecule)
THICKNESS of membrane
SURFACE AREA of membrane
FLUX (dx/dt)
REFLECTION COEFFICIENT
NUMBER OF PARTICLES RETURNED / NUMBER
OF PARTICLES SENT TO MEMBRANE

FICKS EQUATION
Factors that FAVOR diffusion go in the
NUMERATOR
Factors that NEGATIVELY affect diffusion
go in the DENOMINATOR
OTHER FUNCTIONS OF A
MEMBRANE
CREATE and MAINTAIN concentration
gradients
SELECTIVE permeability
Has SATURATED fats( no double bonds)
Has UNSATURATED fats( double bonds)
Easier to break down
Better temperature regulation
More fluidity of movement, especially lateral
ESSENTIAL FATS
Can get them ONLY through the diet
LINOLENIC
LINOLEIC
Used to make ARACHADONIC ACID
Arachadonic acid becomes essential if linoleic
acid is missing from the diet
OTHER MEMBRANE FUNCTIONS
PHAGOCYTOSIS: requires energy
ENDOCYTOSIS: primarily for nutrition
EXOCYTOSIS: primarily for getting rid of
waste products ( i.e. lipofuscin )
PINOCYTOSIS: for movement of fluids and
electrolytes
SKIN is only organ that does this process
72 72
OTHER MEMBRANE FUNCTIONS
TEMPERATURE REGULATION
RADIATION > concentration gradient
CONDUCTION > requires contact
CONVECTION > movement of environment
drags heat out of the body
OTHER MEMBRANE FUNCTIONS
ALL membranes can depolarize
Resting membrane potentials
ELECTROLYTE MOVEMENT

CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)

PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS

TRANSPORT PROTEINS
PRIMARY ACTIVE TRANSPORT
>requires an ATPase. Going against a
gradient
SECONDARY ACTIVE TRANSPORT
Requires sodiums gradient
SYNPORT or COTRANSPORT >moving in
the same direction as sodium
ANTIPORT > movement in opposite direction
as sodium
SECOND MESSENGERS
C-amp > most common second messenger
73 73
PHOSPHODIESTERASE INHIBITORS
CAFFIENE
THEOPHYLLINE
SILDENAFIL
VARDENAFIL
TADALAFIL
SECOND MESSENGERS, cont
IP3 -DAG
IP3-DAG SYSTEM
All HYPOTHALAMIC HORMONES, except
CRH
All SMOOOTH MUSCLE CONTRACTION
by hormone or neurotransmitter
CALCIUM CALMODULIN SYSTEM
4 calcium molecules: 1 calmodulin
All SMOOTH MUSCLE CONTRACTION
by DISTENTION
CALCIUM
Used as a second messenger by
GASTRIN only
TYROSINE KINASE
INSULIN and all GROWTH FACTORS
74 74
NITRIC OXIDE

 NITRIC OXIDE > GUANYLATE CYCLASE

> elevates c-GMP
NITRATES
ENDOTOXIN
ANP
NITRATES
VASODILATORS
TACHYPHYLAXIS; rapid tolerance
Nitroglycerin
Dinilatrate
Sodium Nitroprusside
The End
Insane in the membrane
75 75
INFLAMMATION SHUTTING DOWN THE Na-K ATPase
Potassium still leaks out
Cell becomes more negative > less likely
to depolarize
SHUTTING DOWN THE Na-K ATPase, cont
With Na trapped within the cell, calcium
also gets trapped within the cell
This increases contractility
DIGITALIS
DIGITOXIN
OUBAIN
EKG CHANGES
Na-K ATPase shuts down when a vessel
is 70% stenosed
Potassium leaks out, making cells more
negative
This is why you get ST-wave
DEPRESSION
ST-WAVE DEPRESSION
Early ischemia
70% stenosis
SYMPTOMS BEGIN
Subendocardial ischemia
STABLE ANGINA
Comes on with exertion; goes away with rest
30% flow is enough at rest, but not on exertion
TX: VASODILATORS > increase radius increases
flow
FOLLOW-UP FOR ANGINA

PAIN GOES AWAY

Hospitalize for 24hours
Do serial EKGs and CIEs (Q6h x 24h)
If negative workup, then discharge home
Do a regular STRESS TEST in 6 weeks
Do STRESS THALLIUM test in 6 weeks
Thallium flows through the coronary arteries
Look for COLD AREAS: NO FLOW( ISCHEMIC)

76 76
FOLLOW-UP FOR ANGINA, cont
If you think they might have had an MI,
then do a Ca-PYROPHOSPHATE scan
Cells that die calcify
Dead cells will take up the CaPYROPHOSPHATE
Look for a HOT SPOT
FOLLOW-UP FOR ANGINA, cont
IF PATIENT UNABLE TO PERFORM THE
STRESS TEST:
DOBUTAMINE STRESS TEST
DIPYRIDAMOLE STRESS TEST
EKG CHANGES
Na gets trapped within a cell when there is
at least 90% stenosis
Cells become more POSITIVE
UNSTABLE ANGINA
90% stenosis
EVENTS OCCUR
PLAQUE RUPTURED, and platelets are
closing off the rest of the lumen
TX: Aspirin > Nitrates> Oxygen > Heparin
> tPa > Morphine > B-blockers > Take to
CATH LAB for angiogram
ANGIOGRAM FINDINGS
LEFT MAIN CORONARY ARTERY
OCCLUSION ( 70% stenosis or more)
THREE OR MORE VESSELL DISEASE
TX: GO STRAIGHT TO SURGERY
ANGIOGRAM FINDINGS, cont
ANY SINGLE OR DOUBLE VESSELL
DISEASE
TX: PTCA with STENT placement coated
with CLOPIDOGREL

77 77
CELLS ARE MORE LIKELY TO
DEPOLARIZE WHEN ISCHEMIC
After a stroke: SEIZURES
After an MI: ARRYTHMIAS
After ischemic bowel: BLOODY DIARREA
After a DVT: CRAMPS
WITH Na and Ca trapped within the
cell
Since atria use Ca to depolarize, the
trapped Ca may cause atrial arrythmias
Contractility of muscles increases
WITH CELL DYING,
Sodium continues to accumulate inside
cell
Chloride will follow
WATER will follow next
SWELLING is therefore the FIRST visible
change of cellular injury
SWELLING

Cerebral edema
Papilledema
Hydropic changes
Dilated lymphatics
Third spacing

INFLAMMATION TIME LINE

< 24 hours: SWELLING
AT 24 hours: NEUTROPHILS show up
and peak at 3 days
T-cells and MACROPHAGES: show up at
day 4 and peak at day 7
FIBROBLASTS: show up at day 7, peak at
day 30, and take 3 to 6 months to
complete their work ( chronic
inflammation)
WHEN TOO MUCH SODIUM
INSIDE CELL.
Sodium begins to leak OUT of the cell now
that concentration gradient is reversed
The only way for sodium to get out is to
use the Na-Ca exchange protein which is
concentration driven
78 78
IF BLOOD SUPPLY NEVER
RETURNS TO THE CELL
The sodium can pull ALL the calcium into
the cell
WHILE calcium is moving into cell, more
atrial arrythmias may develop

WHEN ALL CALCIUM NOW

TRAPPED WITHIN THE CELL
Cells that depend on EXTRACELLULAR
calcium will lose function
SMOOTH MUSCLE
ATRIUM
VENTRICLE
SIGN OF CHRONIC DISEASE
ON BIOPSY: you see evidence of fibrosis
ON X-RAY: you see calcifications
ALL inflammatory processes
DONE!!!
79 79
Electrolyte Physiology
Something in the way she moves
me
Electrolyte Movement

CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)
PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS

Electrolyte Movement

CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)
PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS

Electrolyte Movement
CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)
PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS
Electrolyte Movement

CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)
PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS

Electrolyte Movement

CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)
PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS

80 80
Electrolyte Movement

CONCENTRATION GRADIENT
ELECTRICAL GRADIENT
DRIVING FORCE
NERNST NUMBER (E-ion)
CONDUCTANCE (G-ion)
PERMEABILITY
CHANNELS: small ions
PORES: medium-sized molecules (sweat)
TRANSPORT PROTEINS

Electrolyte Movement
Depolarize: to become positive from
baseline
Overshoot: more positive than the
threshold potential
Repolarization: to become negative from a
positive potential
Hyperpolarization ( or undershoot): to
become more negative than baseline
potential
Sodium Channels
81 81
HEART BLOCKS
NORMAL PR-interval : <0.2sec
FIRST DEGREE HEART BLOCK: fixed
and prolonged PR-interval
Problem is AT the SA node or BETWEEN the
SA node and the AV node
NO treatment necessary
Speeding up the heart rate( exercise) will

make the block disappear

HEART BLOCKS, cont
SECOND DEGREE HEART BLOCK
MOBITZ 1: progressive lengthening of PRinterval until QRS is dropped
Early ischemia at the AV node
Also called WENCKEBACKS
Put in pacemaker if symptomatic; do nothing if
asymptomatic
HEART BLOCKS, cont
MOBITZ II: PR-interval is normal; QRS
complexes are dropped erratically
Late ischemia at the AV node
Some cells are negative; some cells are
positive
ALL must have a pacemaker
82 82
HEART BLOCKS, cont
THIRD DEGREE HEART BLOCK
COMPLETE AV DISSOCIATION
AV-node has INFARCTED
P-waves and QRS complexes have NO
relationship
ALL must have a pacemaker
QRS COMPLEXES
Premature ventricular complex (PVC)
No P- wave; wide QRS complex; a pause
following the QRS complex
BIGEMINY: A PVC every other beat
TRIGEMINY: A PVC every third beat
VENTRICULAR TACHYCARDIA: three or
more consecutive PVCs with a minimum heart
rate of 150
VENTRICULAR FIBRILLATION: NO
recognizable QRS complexes
VENTRICULAR TACHYCARDIA
IF PATIENT STABLE: treat with
medication
IF PATIENT UNSTABLE:
SHOCK with 200joules
SHOCK with 300joules
SHOCK with 360(max)joules
LIDOCAINE
SHOCK
BRETYLIUM or AMIODORONE
VENTRICULAR FIBRILLATION
EPINEPHRINE
TREAT LIKE VENTRICULAR

TACHYCARDIA
ATRIAL ARRHYTHMIAS

Premature atrial contraction (PAC)

Multifocal atrial tachycardia
Paroxysmal supraventricular tachcardia
Atrial flutter
Atrial fibrillation
If ACUTE and STABLE: treat with medication
If ACUTE and UNSTABLE: DEFIBRILLATE
If CHRONIC: treat medically; put on coumadin
May defibrillate after minimum 2 weeks on coumadin

TX: use synchronized button

ELECTROLYTES AFFECT
DEPOLARIZATIONS
FOUR SPECIALIZED MEMBRANES
NEURONS
SKELETAL MUSCLES
SMOOTH MUSCLES
CARDIAC MUSCLE
ATRIUM: uses calcium to depolarize
VENTRICLE: uses sodium to depolarize; uses
intracellular calcium to contract; depends on
extracellular calcium to trigger off intracellular
calcium release
83 83
HYPERMAGNESEMIA

LESS LIKELY TO DEPOLARIZE

AFFECTS CALCIUM AND POTASSIUM
GETS IN THE WAY OF SODIUM
TX: IV normal saline; loop diuretic

HYPOMAGNESEMIA

MORE LIKELY TO DEPOLARIZE

AFFECTS CALCIUM and POTASSIUM
AFFECTS all KINASES
TX: magnesium sulphate

HYPERCALCEMIA
LESS LIKELY TO DEPOLARIZE
everywhere except the atrium( more likely)
SMOOTH MUSCLE: initially less likely
(blocks nerve) to depolarize, then more
likely to CONTRACT (due to second
messenger systems)
TX: IV normal saline; loop diuretics
HYPOCALCEMIA
MORE LIKELY TO DEPOLARIZE
everywhere except the atrium( less likely)
WILL AFFECT SECOND MESSENGER

SYSTEMS
SMOOTH MUSCLE: initially more likely to
depolarize( nerve fires more) followed by
less likely to CONTRACT (affects second
messenger systems)
HYPERKALEMIA
Initially MORE LIKELY TO DEPOLARIZE
Potassium will flow into the cell, taking the
membrane potential closer to threshold
Potassium gets trapped INSIDE the cell during
repolarization; repolarization therefore takes
longer > LESS LIKELY TO DEPOLARIZE
Peaked T waves
Widened T waves
Prolonged QT interval
Predisposes to arrythmias
HYPOKALEMIA
LESS LIKELY TO DEPOLARIZE
Potassium will rush out of the cells,
making them more negative
Cells repolarize even faster
Cells repolarize too much
Narrow T waves
Flat T waves
Flipped and inverted T wave
The U wave( exaggerated flipped T wave)
84 84
HYPERNATREMIA
MORE LIKELY TO DEPOLARIZE
SODIUM rushes into the cells, making
them more positive
After sometime, the NA-K ATP-ase kicks
Into high gear, making the cells more
negative( less likely to depolarize)
TX: IV normal saline; correct slowly
HYPONATREMIA
MORE LIKELY TO DEPOLARIZE
SODIUM will now leak out of a cell by Na-K
exchange
When calcium leaks INTO cell in exchange for
sodium leaking OUT, cells become more
positive
TX: IV normal saline; correct slowly
Use 3% saline if sodium under 120 with symptoms
Use fluid restriction if hyponatremia due to SIADH
Hyponatremia The End: Turn off the lytes
Antiarrhythmics
Class 1: Na channel blockers

1a
Quinidine
Procainamide
Disepyramide
1b
Lidocaine
Tocainide
Mixelitine
Phenytoin
1c
Encainide
Flecainide
propofenone
85 85
Class II: Beta Blockers
All end in lol
Specific beta 1: begins with A thru M, but
NOT L or C
Nonspecific: begins with N thru Z,
including L and C
Class II: Beta Blockers

Propanolol Acebutalol
Esmalol Atenalol
Sotalol Pindalol
Timalol
Butexalol
Labetalol
Carvedilol

Class III: K Channel blockers

Napa ( from procainamide)

Sotalol
Bretylium
Amiodorone

Class IV: Ca Channel blocker

Verapamil Quinidine
Diltiazem Procainamide
Nifedipine Phenytoin
Nicardipine
Nimodipine
Femlodipine
Amlodipine

IF YOU PLAY WITH LYTES You may go down IN FLAMES

86 86
PULMONARY PHYSIOLOGY
TAKING A DEEP BREATH
PULMONARY PHYSIOLOGY

Foregut Endoderm
Respiratory Tract
GI Tract > from the mouth to the second
part of the duodenum
Neural Crest
Tracheal cartilage
Laryngeal cartilage
Embryogenesis
Develops in the first trimester like every
other organ
Surfactant production is NOT complete
until approximately 32 to 34 weeks
Brain develops first in embryo: notochord
visible by 3 weeks; brain formed by 8
weeks
Surfactant