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593 Cards in this Set
- Front
- Back
Vitamin A (retinoic acid) deficiency
|
Poor night vision
Hypoparathyroidism |
|
B1 (Thiamine) deficiency
|
Beriberi
Wernecke's Encepahlopathy Wernecke-Korsakoff Syndrome |
|
B2 (Riboflavin) deficinecy
|
Angular cheilosis
|
|
B3 (Niacin) deficinecy
|
4 D's of Pellagra
Diarrhea Dermatitis Dementia Death |
|
B4 (Lipoid Acid) deficiency
|
No deficiency state
|
|
B6 (Pyridoxine) deficiency
|
Neuropathy
|
|
B9 (folate) deficiency
|
Megaloblastic anemia
Hypersegmented neutrophils Neural tube defects |
|
B12 (cyanocobalamin) deficiency
|
Megaloblastic anemia
Hypersegmented neutrophils Neuropathy |
|
Vitamin C (ascorbic acid) deficiency
|
Scurvy
|
|
Vitamin D Deficiency
|
Rickets (Children)
Osteomalacia (adults) |
|
Vitamin E deficiency
|
Increased free radical damage
|
|
Biotin deficiency
|
Loss of carboxylase function
|
|
Vitamin K deficiency
|
Loss of gamma-carboxylation
bleeding |
|
Calcium deficiency
|
Poor bone and teeth development
|
|
MAgnesium deficiency
|
Loss of kinase function
Hypoparathyroidism |
|
Zinc deficiency
|
Dysgeusia
Anosmia Poor wound healing |
|
Copper deficiency
|
Minky kinky hair syndrome
|
|
Iron deficiency
|
Anemia
|
|
Chromium deficiency
|
Diabetes
|
|
Selenium deficiency
|
Dilated cardiomyopathy
|
|
TIn deficiency
|
Poor hair growth
|
|
Molybdenum deficiency
|
Lose xanthine oxidase function
|
|
Manganese deficiency
|
Lose xanthine oxidase function
|
|
Flouride deficiency
|
Poor teeth and bone growth
|
|
Poisons of complex I of the ETC
|
Amytal, ROtenone
|
|
Poisons of complex II of the ETC
|
Malonate
|
|
Poisons of complex III of the ETC
|
Antimycin
|
|
Poisons of complex IV of the ETC
|
CN, CO, Chloramphenicol
|
|
Poisons of complex V of the ETC
|
Oligomycin
|
|
Chemical uncouples of the ETC
|
DNP
Free Fatty Acids |
|
Places where pyruvate feeds into/out of TCA
|
Gly, Ala, Ser
|
|
Places where Acetyl CoA feeds into/out of TCA
|
Phe, Iso, Thr, Tyr, Lys, Leu
|
|
Places where alpha-ketogluterate feeds into/out of TCA
|
Glu, Gln
|
|
Places where succinyl-CoA feeds into/out of TCA
|
Phe, Trp, Tyr
|
|
Places where fumarate feeds into/out of TCA
|
Pro
|
|
Places where oxaloacetate feeds into/out of TCA
|
Asp, Asn
|
|
PKU
|
Phenylalanine hydroxylase deficiency, needed to make tyrosine, leads to a lack of Dopamine, Epi and norepi, melaning, blond/blue/fair, musty odor, Phenylacetate and phenylpyruvate in urine (Guthrie test)
|
|
Maple Syrup Urine Disease
|
Decreased degradation of branched amino acids (Leu, Iso, Val), decreased alpha-ketoacid dehydrogenase, defective transport in the kidney
|
|
Cystinuria
|
Cystathione synthase deficiency, Cys, Ornithine, Lys and Arg end up in urine (COLA), defect in renal tubular transport, cystine stones. Tx: Acetazolamide
|
|
Acidic amino acids
|
Asp Glu
|
|
Basic amino acids
|
Arg Lys
|
|
Amino Acids with O Bonds
|
Ser (90%) Thr Tyr
|
|
Amino acids with N bonds (extra NH2)
|
Asp Gln
|
|
Branched Amino Acids
|
Leu, Iso, Val
|
|
Bulky (aromatic) Amino Acids
|
Phe Tyr Trp
|
|
Smallest Amino Acid
|
GLy
|
|
Amino acid responsible for bends
|
Pro
|
|
CNS excitatory amino acid
|
Asp
|
|
Amino acid that makes catecholamines
|
Tyr
|
|
Ketogenic amino acid
|
Lys Leu
|
|
Gluco and Ketogenic Amino Acids
|
Phe Iso Thr Trp
|
|
Glucogenic Amino acids
|
His, Asn, Val, Arg, Tyr, Ala, Iso, Glu, Cys, Gly, Thr, Asp, Pro, Trp, Gln, Met (Everything except Lys and Leu)
|
|
Essential Amino Acids
|
PVT TIM HALL
Phe, Val, Thr, Trp, Iso, Met, His, Arg, Leu, Lys |
|
If there is a deficiency in Met then what becomes essential?
|
Cys
|
|
Trypsin cuts
|
To the right of Arg, Lys
|
|
Chymotrypsin cuts
|
To the right of Phe, Tyr, Trp
|
|
Elastase cuts
|
To the right of Gly, Ser, Ala
|
|
Mercaptoethanol cuts
|
To the right of Met Cys
|
|
Aminopeptidase cuts
|
The amino terminus
|
|
Carboxypeptidase cuts
|
Left of the carboxyl terminus
|
|
Cyanobromide cuts
|
To the right of Met
|
|
cAMP
|
Sympathetic, Catabolic, CRH
|
|
cGMP
|
Parasympathetic, anabolic
|
|
IP3/DAG
|
Smooth muscle contraction by hormones. Neurotransmitters. All hypothalamic hormones except CRH.
|
|
Ca:Calmodulin
|
Smooth muslce contraction by distention
|
|
Ca++ second messanger
|
Gastrin
|
|
Tyrosine Kinase
|
Insulin and all growth factors
|
|
NO
|
Nitrates, Viagra, ANP and LPS
|
|
Cofactors for Pyruvate Dehydrogenase, alpha-ketoglutarate dehydrogenase and branched-chain dehydrogenase
|
TPP....Thiamine (B1)
Lipoic Acid....B4 CoA....Pantothenic Acid (B5) FAD....Riboflavin....(B2) NAD....Niacin (B3) |
|
Only Imino acid
|
Proline
|
|
Common with all amino acids?
|
THey all have Amino and Acid group
|
|
Define: Dissociate, Soluble, Bioavailable
|
Dissociation: Giving up H+
Soluble: Charged Bioavailable: Uncharged |
|
Best AA buffer in bodies
|
Histidine
|
|
Define anode and cathode
|
Anode: Pole anions go to
Cathode: Pole cations go to |
|
Define isoelectric point
|
Isoelectric point means there is no net charge
|
|
What does ketogenic mean?
|
made from and broken into AcCoA (Avoid in DM)
|
|
What does glucogenic mean?
|
Made from and broken into anything but AcCoA
|
|
Which amino acid is used to make cysteine?
|
Methionine
|
|
Four hormones with disulfide bonds
|
Prolactin
Insulin Inhibin Growth Hormone |
|
Newborn screening diseases
|
PKU
CAH Biotinidase Growth Hormone Hypothyroidism Galactosemia Sickle Cell |
|
Enzyme deficiency in PKU
|
Phenylalanie Hydroxylase
|
|
Signs and symptoms of PKU
|
Musky Odor
Mitral Regurgitation Fair Skin Blue eyes Blond hair |
|
AA deficiency in PKU
|
Tyrosine
|
|
What substances build up?
|
Phenyl-pyruvate
Phenyl-acetate |
|
Treatment for PKU
|
avoid aspartame
|
|
Defect in MSUD
|
Nephron transport protein
|
|
Signs and symptoms of MSUD
|
Sweet urine
|
|
AA's in MSUD
|
Leucine
Isoleucine Valine |
|
Defect in Cysteinurea
|
Cystine, Ornatine, Lysine, Arginine (COLA)
|
|
What crystals are seen in cysteinurea?
|
Coffin lid/envelope shaped
|
|
Amino acids humans have?
|
L-amino acids
|
|
What determines AA primary structure?
|
Amino acid sequences
|
|
What is the primary factor to determine tertiary structure of protein?
|
Hydrophobic/Hydrophilic interaction
|
|
What are the three characteristics of peptide bonds?
|
Planar-flat
Limited rotation Trans configuration |
|
What is characteristic of amino acid quaternary structure?
|
Allosterism (cooperativity)
|
|
For enzymes, define KM and Vmax
|
KM=potency
Vmax= Efficacy Km= 1/2Vmax Km=1/affinity |
|
From what are porphyrin rings made?
|
Succinyl CoA
|
|
Rate limiting enzyme in heme synthesis?
|
Delta Aminolevulonic Acid Synthase (d-ala)
|
|
What are the structure of HbA, A2 and F
|
A- a2b2
A2- a2d2 F- a2g2 |
|
In what percentages do Hb A, A2 and F exist in the body?
|
A- 98%
A2- <2% F- Child <6mos |
|
Enzymes inhibited by lead in Heme synthesis
|
d-Ala, ferrochelatase
|
|
What enzyme adds iron to porphyrin rings?
|
Ferrochelatase
|
|
What buffers Fe2+
|
Histidine
|
|
# of heme sites in 1g of heme
|
4
|
|
Grams of iron in 1 unit of blood
|
3.4
|
|
Acute, intermittent porphyria
|
Recurrent, severe, acute abdominal pain and neuropathies
|
|
Clues for porphyria cutanea tarda
|
Blisters with light
Onset >5yrs |
|
Clues for erythrocytic protoporphyria
|
Blisters with light, onset <5yrs
|
|
Rx for AIP
|
Fluids, Sugar, Hematin
|
|
What is the defect in all thalassemias?
|
Gene deletion
|
|
# of genese for alpha and beta subunits of Hb
|
Alpha-4
Beta-2 |
|
Define thalassemia major/minor
|
Minor: 1 gene left
Major: No genes left |
|
Alpha thalassemia minor 1 gene deleted
|
asymptomatic
|
|
Alpha thalassemia minor 2 genes deleted
|
Active- symptomatice
Not Active- asymptomatic Hb Bart Beta Tetramer |
|
Alpha thalassemia minor 3 genese deleted
|
Symptomatic
|
|
Alpha thalassemia major
|
4 genes deleted
hydrops fetalis |
|
Beta thalassemia minor
|
+/- symptoms
Ok until 4-6 months |
|
Beta thalassemia major
|
always symptomatic
Transfusion dependent Only Hg A2 and F Cooley's anemia |
|
What is cooley's anemia?
|
Big Skull
Hepatosplenomegaly Big sternum Big pelvis |
|
Causes of right shift of the Oxy-Hb Curve
|
Hypoxia
Increased lactic acid Increased 2,3 BPG Increased [H] Increased temperature Increased altitude Increased exercise Decreased pH Increased pCO2 |
|
Released from muscle cells during Rhabdomyolysis
|
Myoglobin
|
|
Carbon monoxide
|
Competitive inhibitor
Binds 200X stronger than O2 SaO2 is high pO2 is low |
|
Rx for CO poisoning
|
Hyperbaric O2
|
|
Cyanide
|
non-competitive inhibitor
pO2 is normal SaO2 is low |
|
MCC of cyanide poisoning
|
Na Nitroprusside used for hypertensive crisis
|
|
Rx for cyanide poisoning
|
Amylnitrate --> Fe2+-->Fe3+
Thiosulfate-->Thiocyanate Methylene Blue Fe3--->Fe2 |
|
Rx methemoglobinemia
|
Methylene Blue
|
|
What causes primary methemoglobinemia?
|
Congenital
|
|
What causes secondary methemoglobinemia?
|
Drugs, MC: Sulfa
|
|
What is the pO2 ans SaO2 for methemoglobinemia?
|
pO2 is normal
SaO2 is low |
|
Effect of hydrolysis on proteins
|
Denatures protein
Change ANS--> ASP Change glutamate to Aspartic acid and glutamic acid |
|
How does gel electrophoresis work?
|
Separates by size
Separates by charge |
|
Trypsin cuts to the right of
|
Lysine, Arginine
|
|
4 most abundant collagen types
|
I-S- Skin and Bone
II- C- Connective tissue III- A- Arteries IV- B- Basement membrane |
|
What protein is defective in Marfans?
|
Fibrilin
|
|
Clues for Marfans
|
Wingspan > Height
Arachondactyly Lens dislocation from bottom |
|
Clues for Ehrler's Danlos
|
Hyperstretchable skin
|
|
How does homocystein work?
|
INH lysine hydroxylase --> inhibits collagen synthesis
|
|
Clue for homoocysteinurea
|
Dislocation of lens from top
|
|
What is the defect in scurvy?
|
Vit C is needed to hydroxylate Lsy and Pro in collagen synthesis
|
|
Clues for scurvy
|
Gingival bleeding
Perifollicular hemmorhages |
|
Clues for syphilis
|
Obliterative endarteritis
Tree barking Shooting, Lancinating pain |
|
Clues for congenital Syphillis
|
Anterior bowing of the legs
Snuffles Hutchinson's teeth |
|
Defect in minky kinky hair disease
|
Cu2+ deficiency
|
|
Clues for minky kinky hair disease
|
Hair looks like copper
Hair cuts the face |
|
Differentiate OI from abuse
|
OI-->shattering fracture
|
|
In what population do you see Takayasu disease?
|
Asian women
|
|
What is Takayasu?
|
Granulomatous Aortitis
|
|
What is the only protein modified in the ER?
|
Collagen
|
|
What are the Amino acids found in collagen?
|
Gly, Pro, Lys
|
|
What vitamin is needed for collagen syn?
|
Vitamin C
|
|
What other mineral is required for collagen?
|
Copper
|
|
What two AAs are hydroxylated in collagen?
|
Proline, Lysine
|
|
How do all proteins begin?
|
pre-pro protein
|
|
In what form is collagen secreted? What happens after secretion?
|
Collagen is secreted from the GOLGI as tropocollagen and a cytoplasmic peptidase cleaves off OH
|
|
Where do each of the following guide a protein?
|
Pre- ER
Pro- Golgi Mannose-6-Phosphate- Lysosomes Short amino terminus sequence- Mitochondria |
|
Difference between elastin and collagen?
|
Elastin has no OH-lysine
|
|
What gives elastin elasticity?
|
Desomsine--> 4 lysines
|
|
Enzymes that breaks down elastin?
|
Elastase
|
|
2 bacteria with elastase?
|
Staph, Pseudomonas
|
|
What provides tensil strength?
|
Keratin
|
|
Kinds of bonds in Keratin
|
Disulfide
|
|
ETC complex needing iron?
|
III and IV
|
|
ETC complex needing Cu
|
III
|
|
FADH2/NADH feed into ETC at....
|
FADH2--> Complex II
NADH--> Complex I |
|
Inhibiting ETC means
|
stop electron transport and stop heat generation
|
|
Uncouple ETC means
|
Stop electron transport but heat generation continues
|
|
Who has uncoupled ETC
|
babys and polar bears
|
|
Types of sugars and AAs in humans
|
L-Sugars
D-Amino Acids |
|
Why does the body phosphorylate things?
|
To keep them inside cells
|
|
What are the regulatory enzymes of glycolysis?
|
Hexokinase, PFK1, Pyruvate Kinase
|
|
Glucokinase in found where?
|
Liver and Pancreas after a meal
|
|
Hexokinase is found where?
|
Everywhere
|
|
7 places not requiring insulin to take up glucose?
|
B-Brain
R-RBC I-Intestinal Wall C-Cornea K-Kidney L-Liver E-Exercising Muscle |
|
3 Enzymes needing B1
|
Pyruvate Dehydrogenase
Alpha Ketoglutarate Dehydrogenase BCAA Dehydrogenase |
|
B1
|
Thiamine
|
|
B2
|
Riboflavin
|
|
B3
|
Niacin
|
|
B4
|
Lipoic Acid
|
|
B5
|
Pantothenic Acid
|
|
B6
|
Pryladoxime
|
|
B9
|
Folate
|
|
B12
|
Cyanocobalomine
|
|
Diseases like Pellagra
|
Hartnup
|
|
Source of B2
|
Milk
|
|
What breaks down B2
|
Sunlight
|
|
What cannot be transported in Hartnup?
|
Tryptophan
|
|
5 Fates of Pyruvate
|
Lactic Acid
Alanine OAA AcCoA EtOH |
|
Enzymes for the five fates of Pyruvate
|
Lactate dehydrogenase
Alanine Transferase (ALT) Pyruvate Carboxylase Pyruvate Dehydrogenase Ethanol Dehydrogenase |
|
Viral vs EtOH Hepatitis
|
Viral 1:1 AST/ALT
Alcoholic >2:1 AST/ALT |
|
Explain AST:ALT ratio
|
AST in cyto & Mito
ALT only in Cyto Viruses: attack membrane, 1:1 Alcohol also attacks Mitochondria |
|
Drugs causing disulfram rxn
|
Disulfram and metronidazole
|
|
Mercury inhibits
|
G3P Kinase
|
|
Flouride Inhibits
|
Enolase
|
|
Sings of flouride poisoning
|
Perly white teeth and bones
|
|
TCA enzyme connected to ETC
|
Succinyl-CoA Dehydrogenase is connected at complex II
|
|
Enzymes in Glycolysis
|
Glucose/Hexokinase
Glucose 6 P Isomerase Fructose 6-P Kinase Aldolase A GA3P Kinase 1,3 Bisphosphoguconate DH 3PG Isomerase Enolase Pyruvate Kinase |
|
4 Regulatory Enzymes in Gluconeogenesis
|
Pyruvate Carboxylase
PEPCK Fructose 1,6 bisphosphatase Glucose-6- Phosphatase |
|
Intermediates in TCA
|
"Cindy Is Kinky So She Fornicates More Often"
Acetyl CoA Citrate Isocitrate Alpha Ketoglutarate Succinyl CoA Succinate Fumarate Malate Oxaloacetate |
|
Intermediates in Urea Cycle
|
NH4+ CO2+ ATP
Carbomyl-P + Ornithine Citrulline + Asp Arginosuccinate-Fumarate L-Arginine+ Fumarate Ornithine+ Urea |
|
Intermediates in Pentose Phosphate Pathway
|
Glucose, G-6-P, Phosphogluconate, Ribulose 5 P
|
|
Intermediates in Fructose Catabolism
|
Fructose, Fructose 1 P, DHAP/Glycerol
|
|
Deficiency in Fructosuira
|
Fructokinase
|
|
Deficiency in Fructosemia
|
Aldolase B
|
|
Deficiency in Galactosuria
|
Galactokinase
|
|
Deficiency in Galactosemia
|
Galactose-1-Uridyl-Transferase
|
|
Complications of Fructosuria/Galactosuria
|
Polydypsia, Polyuria, UTI
|
|
Carriers in Body
|
UDP-Single Sugar
Dolichol-Many Sugars Biotin- CO2 THF- CH3 for nucleus SAM- CH3 for everything else CDP- AA |
|
Excess Sugars
|
Glu --> Sorbitol
Fructose --> Fructicol Galactose -->Galacticol |
|
What is characteristic of a cell membrane?
|
It is a lipid bilayer
|
|
Define Amphipathic
|
Fat soluble and water soluble
|
|
Where will you find hydrophobic/hydrophilic substances?
|
Hydrophobic: Inside
Hydrophilic: Outside |
|
3 exceptions to water out fat in rule
|
Channels
Pores Transmembrane Proteins |
|
RDA for fat/carb/protein
|
30% fat
30% protein 40% carbs |
|
7 Functions of Cell Membranes
|
Provide Structure (#1)
Transport Active Transport Heat/Temp Regulation Maintain Gradient Depolarization Signal transduction |
|
Membrane transport in a cell is called
|
Phagocytosis
|
|
Bringing something into the cell is called
|
Endocytosis
|
|
Putting something outside the cell is called
|
Exocytosis
|
|
Bringing water inside a cell is called
|
Pinocytosis
|
|
What 2 things are required for cellular transport?
|
ATP and Actin
|
|
Most important waste product produced by cells
|
Lipofuscin (Brown Pigment)
|
|
How do you get lipofuscin? What is the cause?
|
With age you become less able to push lipofuscin out of the cell
|
|
What are the two types of active transport?
|
Primary and secondary
|
|
What is the most important factor in the movement of particles?
|
Concentration gradient
|
|
How do you concentrate any substance in the body?
|
With an ATPase
|
|
How does secondary active transport work?
|
Going with the concentration gradient using another substance's gradient
|
|
Most common gradient used for secondary active transport?
|
Sodium
|
|
Secondary active transport in the same/opposite direction is called
|
Same: cotransport/symport
Opposite: Antiport |
|
Is the cell membrane mostly fats or water?
|
Mostly fat
|
|
What substances cross the membrane more?
|
Fat Soluble
|
|
What limits crossing membranes?
|
Concentration gradient
|
|
Where are fat soluble hormone/steroid hormone receptors?
|
Nucleus. Cortisol is the exception, its receptor is located in the cytoplasm.
|
|
How do you differentiate between one fat soluble hormone and another?
|
You differentiate between them by the proteins that they make.
|
|
Factors that affect transportation of water-soluble compounds or hormones?
|
Size, Charge, pH, Surface area, Membrane thickness, Flux, Reflection coefficient, Fick's Law.
|
|
Principle behind the reflection coefficient?
|
THe reflection coefficient is a ratio of particles sent to particles returned. THat is, if 10 are sent and 10 are returned, that means the reflection coefficient is 1 and impermeable. If 10 are sent and none return, that is a coefficient of 0 or soluble.
|
|
What is the principle behind Fick's law?
|
Ratio of things that promote corssing a membrane to things that inhibit crossing membrane
|
|
How do ions cross membranes?
|
Channels
|
|
How medium particles cross membranes?
|
Pores
|
|
How larger molecules cross membranes?
|
Transport protiens
|
|
What are the three ways heat is regulated by the body?
|
Radiation-->into environment
Conduction-->contact Convection-->environment moves past you |
|
How the body gets rid of heat?
|
Vasodilation
|
|
HOw the body keeps heat
|
Vasoconstriction
|
|
Most important substance that is transported thorugh pores?
|
Sweat (NaCl and H2O)
|
|
What hormones have membrane receptors?
|
NON-STEROID HORMONES
|
|
Hormones that have nuclear membrane receptors?
|
All steroid hormones except cortisol which has a cytoplasmic receptor
|
|
How does the cell membrane help the body maintain electrochemical gradients?
|
By keeping ions on the correct side of the membrane to maintain electrical gradient.
|
|
What is the most common extracellular cation/anion?
|
Cation: Sodium
Anion: Chloride |
|
What is the most common intracellular cation/anion?
|
Cation: Potassium
Anion: Proteins |
|
What membranes of the body do not depolarize?
|
Dead membranes
|
|
What membranes of the body are best at depolarizing?
|
Neurons: Purkinje fibers
|
|
What is the most common complication of electrocution?
|
MC complication is bleeding because election causes damage to endothelium but you cannot clot completely because endothelium is damaged.
|
|
What tissues are you most worried about from an electrocution injury?
|
Brain and heart because you develop arrhythmias and seizures
|
|
In 1st 24 hours what is a concern after electrocution?
|
Arrythmias and Seizures
|
|
What type of hormones have 2nd messenger systemss?
|
Water soluble--Protein
|
|
What is the reflection coefficient of protein hormones?
|
Close to 1
|
|
What is the action of cAMP?
|
2nd messanger for sympathetics
|
|
What is the action of cGMP?
|
2nd messenger for parasympathetics
|
|
What is the action of IP3/DAG?
|
Second messenger for all hypothalamic hormones except CRH, and all smooth muscle contraction done by hormones
|
|
Action of Calcium-Calmodulin?
|
Second messenger for all smooth muscle contraction by distention
|
|
Action of Ca2+ as a second messenger?
|
Second messenger for Gastrin
|
|
Action of Tyrosine Kinase
|
2nd messenger for insulin and all growth factors
|
|
Action of nitric oxide
|
2nd messenger for Nitrates
|
|
MC second messenger system
|
cAMP
|
|
How does cAMP system work?
|
Hormone binds R cell---> G Protein disassembles--->alpha subunit activates adenylate cyclase converting ATP to AMP--->AMP activates Protein Kinase A which phosphorylates proteins
|
|
Hormones activated/deactivated by phosphorylation
|
All catabolic are activated by phosphorylation (i.e. glucagon, epi etc).
All anabolic are deactivated by phosphorylation ie. insulin |
|
Enzyme that breaks down cAMP
|
Phosphodiesterase breaks down cAMP
|
|
2 substances that inhibit phosphodiesterase?
|
Caffeine
Theophylline |
|
2 bacteria that ADP-Ribosylate Gs subunit of the G Protein
|
ETEC
VIbrio |
|
Bacteria that ADP-Ribosylate Gi subunit of the G protein
|
Pertussis
|
|
2 bacteria that ADP-Ribosylate EF2
|
Diptheria
Pseudomonas |
|
How does the IP3/DAG system work?
|
Hormone binds to receptor on cell membrane. Phospholipase C splits PIP into IP3 and DAG. IP3 goes to SR and causes release of Calcium. DAG binds to calcium released from SR and activates Protein Kinase C
|
|
How does Nitric Oxide work?
|
Increases Guanylate Cyclase
|
|
Ratio of calcium to calmodulin in the calcium/calmodulin system
|
Four calcium to one calmodulin
|
|
3 second messenger systems enhanced by increased calcium
|
IP3/DAG
Calcium/Calmodulin Calcium |
|
What are the signs and symptoms of nitrates? Why do you see these side effects?
|
HA, Flushing, Nausea/Vomiting, Peripheral edema. YOu see these because nitrates vaso and veno dilate causign increased blood flow to these areas
|
|
Along with nitrates what hypertensive medication both vaso and veno dilates?
|
ACE-Inhibitors
|
|
Why do you get tachyphylaxis with nitrates?
|
Because you develop tolerence due to down regulation of receptors.
|
|
How do you prevent tachyphylaxis caused by nitrates?
|
To prevent, give a daily period off the nitrates (8 hours)
|
|
What substances use nitric oxide as a second messenger?
|
ANP, Endotoxin, Viagra (sildenafil), All nitrates
|
|
For what medical conditions are nitrates used?
|
CHF, acute MI, Angina
|
|
Nitrate used to treat cyanihe poisoning?
|
Amyl Nitrate
|
|
Nitrate given IV/sublingual for chest pain
|
Nitroglycerine
|
|
Nitrate used in the tx of hypertensive crisis
|
Sodium nitroprusside
|
|
FUnction of Smooth endoplasmic reticulum
|
Detoxification
Steroid synthesis |
|
FUnction of Rough Endoplasmic Reticulum
|
Makes proteins for packaging and exocytosis
|
|
Function of free Ribosome
|
Makes proteins for cytoplasm
|
|
Function of lysosome
|
Degradation of waste
|
|
Function of Golgi
|
Post translational modification of proteins
|
|
FUnction of mitochondria
|
Makes energy
|
|
Function of Nucleolus
|
Produces Ribosomal RNA
|
|
Damage to what 3 organelles is irreversible
|
Nuclues, Mitochondira, Lysosomes
|
|
What organ uses sER for detoxification? Which organ uses sER for steroid syn?
|
Detox: Kidney
Steroid syn: Liver |
|
What is the only protein that is modified in the rER?
|
COllagen
|
|
Where are all proteins except collagen modified?
|
Golgi
|
|
Tissues with the most sER?
|
LIver, Kidney
|
|
What substances to lysosomes have a lot of?
|
Acid hydrolases
|
|
What do acid hydrolases do to the pH of lysosmes?
|
Cause the pH to be very acidic
|
|
Structure that is formed when lysosomes phagocytose something?
|
Phagosome or Phagolysosome
|
|
Bacteria that can inhibit phagocytosis by PMNs?
|
TB
|
|
TB component that prevent phagocytosis
|
Cord Factor
|
|
Ion that damages lysosomes by coating their surface?
|
Calcium
|
|
Damage to lysosomes causes
|
Acid hydrolases to leak out and damage the nucleus particularly DNAse and RNAse
|
|
Where do synthetic processes occur in a cell?
|
THe cytoplasm. i.e. glycolysis and glycogen synthesis
|
|
Where do all catabolic processes occur in the body?
|
In the mitochondria (eg TCA, glycogenolysis, fatty acid breakdown)
|
|
Most important primary active transport system?
|
Sodium ATPase (3Na+ out, 2K+ in)
|
|
MOst important secondary active transport system?
|
Sodium calcium exchanger. (3Na+ out, 2Ca2+ in)
|
|
Transport system used to make the cell more negative? More positive?
|
Negative--> Na-K ATPase
Positive-->Na-Ca exchanger |
|
What does a lysosomal inclusion body indicate?
|
Missing enzyme --->inability to digest the substance
|
|
Surface at which proteins enter and leave the Golgi?
|
Enter-->Concave side
Exit--> Convex side |
|
Which parent transmits mitochondrial DNA?
|
Mother
|
|
What is the only important mitochondrial disease?
|
LEBER
|
|
What is the function of polymerase alpha?
|
Primase
|
|
What is the function of polymerase beta?
|
DNA Polymerase I
|
|
What is the function of Polymerase gamma?
|
Mitochondrial DNA
|
|
What is the function of polymerase delta?
|
DNA Polymerase III
|
|
What is the function of polymerase epsilon?
|
DNA Polymerase III
|
|
What is the outcome of all chromosomal abnormalities?
|
They ALL DIE
|
|
Monosomy that does not die
|
Turner's
|
|
Major concept behind monosomies?
|
If they do not die, things won't grow
|
|
What are the unique features of Turner's?
|
Web neck: Neck did not grow so they have extra skin
Cystic hygroma: Brachial pouches did not develop Shield Chest: Waist did not grow Gonadal streaks: Ovaries did not grow Coarctation of the Aorta: Aortic arch did not grow |
|
Cules for coarctation?
|
Differential pulses
Differential cyanosis Rib notching on X-Ray |
|
Reason for rib notching in coarctation?
|
Bronchial arteries open up to allow blood to flow and eroding ribs
|
|
Reason for differential cyanosis in coarctation?
|
The PDA joins distal to coarctation
|
|
Name the trisomies
|
13-Patau
18- Edwards 21: Downs |
|
Clues for Patau
|
Die shortly after birth
Puberty High arched Palate Polydactyly P-System |
|
Clues for Edwards
|
Die shortly after birth
95% have rocker bottom feet |
|
8 Features of Down's
|
MR
20-50% congenital heart dz 40% hypothyroidism Cancer: ALL Early onset Alzheimers Simian crease Mongolian Slant Wide spaced 1st and 2nd toe |
|
MC congenital heart disease in down's?
|
Common AV canal
ASD and VSD together VSD only ASD only |
|
To what is a common AV Canal due?
|
Failure of endocardial cushion to develop
|
|
MC cyanotic heart disease in Down's?
|
Tetralogy of Fallot
|
|
Most common/frequent cancer seen in down's?
|
Common: ALL
Frequent: AML |
|
List the IQ scale
|
Genius >130
Normal 85-100 Mild MR: 70 Moderate MR: 55 Severe MR: 40 Profound MR: <25 |
|
Level of MR that requires institutionalization?
|
<25 Profound
|
|
Which type of memory is affected first in Alzheimer's dz?
|
Short term memory because Alzheimer's affects the hippocampus first
|
|
What tissue change is the hallmark of Alzheimer's disease?
|
Neurofibrillary tangles in the brain
|
|
Neurotransmitter that is decreased in Alzheimers?
|
Ach
|
|
What enzyme makes the Ach that is decreased in Alzheimers?
|
Choline acetyl transferase
|
|
Drug used to treat Alzheimers that inhibits the breakdown of Ach
|
Tacrine inhibits the breakdown of Ach
|
|
3 types of nuclear damage and a description of the nucleus
|
Pyknosis: Blobs
aryorrhexis: Chunks Karryolysis: Dissolves |
|
Describe coagulative necrosis
|
Due to ischemia, architecture is maintained
|
|
Describe liquefactive necrosis
|
1/2 solid 1/2 liquid. No maintenance of architecture. i.e. brain abscess
|
|
Describe hemmorhagic necrosis
|
Organs with soft capsules or more than one blood supply
|
|
Describe caseous necrosis
|
Cheesy, TB only
|
|
Describe Fat Necrosis
|
Occurs in the pancreas with chronic pancreatitis, or in blunt trauma to the breast
|
|
Describe purulent necrosis
|
Pus due to bacteria (PMN)
|
|
Describe granulomatous necrosis
|
Granulomas
T-Cells/Macrophages Non-Bacterial |
|
Describe fibrinous necrosis
|
Collagen vascular disease. uremia. TB
|
|
2 types of cellular death. What is the difference and how can you differentiate between the two?
|
Apoptosis: Programmed cell death
Necrosis: non-programmed cell death Necrosis has inflammation and apoptosis does not |
|
MCC of necrosis
|
Ischemia leading to coagulative necrosis
|
|
What is the theory behind chemotherapy? What is responsible for the side effects of chemotherpay?
|
Try to kill the cancer before cancer or drug kills the patient. Targets features of the cancer cell that normal cells are not doing, i.e. rapidly dividing.
|
|
What are the five classes of chemotherapy drugs?
|
Nutrient depleater
Antimetabolites Alkylating agents Microtubule inhibitors Immune Modulators |
|
3 Chemotheraputic drugs that inhibit dihydrofolate reductase
|
Trimethoprim
Pyrimethamine Methotrexate |
|
What happens to the cell if you stop the Na/K pump?
|
Potassium leaks out and the cell becomes negative. Sodium moves down the concentration gradient into the cell. Chloride follows sodium into the cell and so does water. The cell begins to swell.
|
|
What is swelling called in the brain, liver and any other cell
|
Brain: Papilledema
Liver: Balloon degenration Other: Hydropic changes |
|
3 substances that inhibit the sodium potassium pump?
|
Digitalis
Digitoxin Ouabain |
|
Normal resting membrane potential for cells?
|
(-90)
|
|
What cells do not sit at the normal resting membrane potential? Are they more or less likely to depolarize?
|
Neurons and Purkinje fibers have a resting membrane potential of (-70). They are more likely to depolarize.
|
|
What is the Nerst number?
|
The membrane potential at which the electrical and concentration gradient are equal and opposite. THis means there is no NET movement.
|
|
What is the Nerst number for: Na, K, Cl, Mg, and Ca
|
Na (+65)
Cl (-90) K (-96) Mg2+ (+120) Ca2+ (+120) |
|
What determines electrical gradient?
|
The direction ions want to go into order to get to its own E
|
|
By electrical and concentration gradient, which way do the following ions want to flow? Na, K, Cl
|
Na: In (-90) to (+65)
K: Out (-90) to (-96) Cl: Alread at its E |
|
Which vessel has the thickest layer of smooth muscle?
|
Aorta
|
|
Which vessels have the largest cross sectional area of smooth muscle?
|
Arterioles
|
|
Which vessels have the largest cross sectional area?
|
Capillaries
|
|
Which vessels can store the most blood?
|
Veins and venules
|
|
Which vessels have the thinnest walls?
|
Capillaries
|
|
Which vessel has the greatest amount of diffusion?
|
Capillaries
|
|
How does the body maintain stroke volume during hypovolemic shock?
|
By constricting the veins and venules.
|
|
How much blood is stored in the veins and venules?
|
Sixty percent of the blood
|
|
Vessels in which most diffusion occurs?
|
Capillaries
|
|
Type of epithelium that makes up the aorta?
|
Stratified squamous
|
|
Calcification of the aortic arch due to trauma and age is called
|
Monckeberg calcification
|
|
What gives veins and venules such great compliance?
|
Elastin
|
|
What two factors help overcome afterload and deliver blood to tissues?
|
Ventricular contraction and aortic recoil.
|
|
What three factors prevent blood from being delivered to the heart during systole?
|
Aortic valves partially occlude coronary vessels
There is no transmural force pushing the coronary blood vessels The contracting ventricles compress the coronary vessels |
|
How much O2 is extracted from blood by the heart?
|
97%
|
|
With fast heart rates, in which phase of the cycle does the heart spend most time in: systole or diastole? With slow heart rates is more time spent in systole or diastole?
|
Fast heart rates: more time spent in systole.
Slow heart rates: more time in diastole |
|
As you age what happens to the aorta?
|
The aorta calcifies
|
|
How does calcification of the aorta affect compliance?
|
Compliance decreases
|
|
What is the effect of calcification of the aorta on blood pressure and pulse pressure?
|
Blood pressure increases (mainly systolic). Puls pressure increases (systolic increases, diastolic remains relativley unchanged)
|
|
How do you treat hypertension in the elderly?
|
Calcium channel blockers
|
|
What two organs of the body have resistence of vessels in series?
|
Kidney and liver
|
|
Why do the liver and kidney have resistence of vessels in series?
|
They detoxify blood so you want blood to move slowly. Even though the velocity of the downstream blood is increased, there is a basckup of blood so blood flow decreases and the blood spends more time being detoxified.
|
|
Vasodilators of the organs
|
Brain: Increased PCO2, Decreased P02
CV: Adenosine Lung: Increased PO2 Muscles: Increased PCO2, Decreased pH GI: Food (esp fat) Skin: Increased Temp, Increased pCO2 Renal: D2 Receptors, Prostaglandins, ANP |
|
How does decreased O2 cause pulmonary HTN?
|
Decreased O2 causes vasoconstriction leading to pulmonary hypertension
|
|
Name for obstructive sleep apnea due to obesity?
|
Pickwickian syndrome
|
|
What is the function of the carotid body? Carotid sinus?
|
Carotid sinus is a baroreceptor. It measures the stroke volume.
Carotid body is a chemoreceptor. |
|
What is the pathway of signals from the carotid sinus?
|
Carotid sinus measures stroke volume. It sends signal to Nuclues tractus Solitariusw in the medulla via CN IX. The medulla then sends a signal to the heart via CN X. Medulla causes increased release of norepi.
|
|
How does the carotid sinus affect firing of CN IX and X?
|
Cranial nerves IX and X are always firing.
Firing goes up or down with the stroke volume. Norepinephrine goes in the opposite direciton. Increased stroke volume causes increased firing of IX and X. Decreased stroke volume causes decreased firing of IX and X |
|
What affect does CN X have on the heart?
|
CN X is inhibitory to the heart. Increased firing causes decreased heart rate. Decreased firing causes increased heart rate.
|
|
When you stand up how much does your heart rate and blood pressure change?
|
HR increased by 5-10 bpm. BP drops by 5-20 mmHg
|
|
What is the meaning of a change in HR/BP upon standing of less than expected?
|
A change of HR of less than 5bpm means your body did not respond. Autonomic dysfunction.
|
|
What is the meaning of a change in HR/BP upon standing of greater than expected?
|
A change of more than 10 bpm means your body overcompensated. Volume depletion.
|
|
Four instances of autonomic dysfunction
|
Baby: Reily Day Syn
Diabetics: Neuropathy Parkinson: Shy-Drager Elderly: Sick sinus syndrome |
|
What is the pathology of sick sinus syndrome in the elderly?
|
Carotid sinus is so calcified that it is not responding. Sick sinus means pausing for more than one second.
|
|
What is the pathology of Reily Day Syndrome?
|
Babies are born with no autonomic reflexes.
|
|
With respect to the carotid sinus, what sequence of events takes place when you increased your fluid volume?
|
Carotid sinus increases firing. CN IX and X increase firing. HR Decreases (Reflex bradycardia)
|
|
Sequence of events that takes place when you stand from a seated position (carotid sinus).
|
Blood pools in legs
Decreased venous return Decreased EDV Decreased stroke volume Decreased firing of carotid sinus Decreased firing of CN IX and X Increased HR (Reflex tachycardia) Decreased BP 5-20mmHg Increased HR 5-10 bpm |
|
Mechanism responsible for immediate regulation of BP
|
Carotid reflex via carotid sinus
|
|
Mechanism responsible for intermediate regulation of BP?
|
Norepinephrine (Alpha 1 then beta 1 receptors)
|
|
Mechanism responsible for long term regulation of blood pressure?
|
Kidney
|
|
What substance is the most potent vasoconstrictor in the body?
|
Angiotensin II
|
|
To what stimulus do JG cells in the kidney respond? What is their response?
|
They respond to flow i.e. volume, not pressure. This causes the release of Renin.
|
|
What is the rationale for using a carotid massage?
|
Massaging the carotid sinus stimulates an increase in stroke volume. This causes increased firing of the carotid sinus, increased firing of CN IX and X and decrease in HR.
|
|
How does norepinephrine regulate blood pressure?
|
If carotid reflex is not enough to normalize BP, NE is released and causes vasoconstriction via alpha 1 receptors and increase in HR by beta 1 receptors.
|
|
What is the function of the carotid reflex?
|
THe carotid sinus is responsible for immediate regulation of BP via reflex Brady and Tachy.
|
|
What is the dx for a patient presenting with increased HR and normal BP?
|
Hypovolemia (Compensated shock)
|
|
What are the first physical signs of hypovolemia?
|
First signs are poor skin turgor (mottled skin), increased pulse, and decreased bowel sounds.
|
|
What is lentigo reticularis?
|
Hypoperfusion of the skin due to vasoconstriction or shock.
|
|
Two most important actions of angiotensin II?
|
Vasoconstriction
Stimulate Aldosterone Release |
|
Aldosterone electrolyte resposne
|
Aldosterone causes reabsorption of sodium and excretionj of potassium in kidney, but reabsorbs 3x more water than sodium & secretion of H+
|
|
What are the electrolytes, pH, TPR, and BP for all low volume states?
|
Low K, Na, Cl, H+
|
|
What are the 3 exceptions to the rule of all electrolytes for low volume states?
|
Diarrhea (Pooping HCO3)
RTA (peeing HCO3) DKA (Ketones) THese have the same electrolytes but HIGH H+ |
|
What is the tx for HTN in CHF?
|
ACE-Inhibitor
|
|
Heart block with fixed lengthening of PR interval?
|
First Degree
|
|
HEart block with normal PR interval and erratic loss of QRS?
|
Second degree (Mobitz 2)
|
|
Heart block with gradual lengthening of PR interval and erratic loss of QRS?
|
Second degree Mobitz I
|
|
How do you treat the various types of heart block?
|
1st degree: no tx
Mobitz 1: Pacer if sxs Mobitz 2: Pacer Mobitz 3: Pacer |
|
Complication of temporal arteritis?
|
Blindness
|
|
Another name for temporal arteritis?
|
Giant cell arteritis
|
|
how do you diagnose temporal arteritis?
|
Temporal artery biopsy
|
|
Rule of 60's for Temporal Arteritis?
|
Age >60
ESR>60 60 mg prednisone tx |
|
Which should you do first in temporal arteritis: biopsy or steroids
|
If symptomatic, tx with prednisone then biopsy. If asymptomatic, biopsy then prednisone.
|
|
Myositis
|
One muscle hurt
|
|
Several muscles hurt
|
Polymyositis
|
|
Muscle pain with rash
|
Dermatomyositis
|
|
Inflammed muscle insertions
|
Fibrositis
|
|
Pain of muscle and muscle insertions
|
Fibromyalgia
|
|
Shoulder girdle hurts most
|
Polymyalgia Rheumatica
|
|
Visceral cancer muscle condition
|
Dermatomyositis
|
|
Drugs that cause myositis
|
Rifampin
INH Statins Prednison |
|
Muscle condition treated with amitryptaline
|
Fibromyalgia
|
|
Increased incidence in temporal arteritis
|
Polymyalgia Rheumatica
|
|
Muscle condition with multiple trigger points
|
Fibromyalgia
|
|
Muscle pain when moving
|
Fibrositis
|
|
Heliotropic muscle pain
|
Dermatomyositis
|
|
Throbbing temporal headache
|
Temporal Arteritis
|
|
Disease that causes myositis
|
Hypothyroidism
|
|
3 clues for Becker's or Duchenne's muscular dystrophy
|
Waddling Gate
Gower's sign Calf Pseudohypertrophy |
|
Causes of pseudohypertrophy seen in the calfs of Duchennes or Becker's
|
Fat deposition in the muslces of the calf
|
|
What is the tx of MS?
|
1) Steroids
2) Blocking Immunoglobulins 3) Plasmapheresis |
|
What is responsbile for the halo vision seen in MS?
|
Optic Neuritis
|
|
What structure do MS like to attack?
|
Medial Longitudinal Fasciculus
|
|
What is Optic Neuritis in MS called?
|
Internuclear opthalmoplegia
|
|
Clues for Duchenne's muscular dystrophy?
|
X-Recessive
Onset before age 5 |
|
Clues for Becker's muscular dystrophy?
|
Onset after age 5
|
|
Ascending paralysis 2 weeks after URI?
|
Guillen Barre
|
|
Clues for myotonic dystrophy
|
Increased muscle tone
Bird Beak face Cannot let go after shaking hands |
|
Neuropathy in glove and stocking distribution?
|
Diabetic neuropathy
|
|
Disease with lancinating, shooting, stabbin pain
|
Shyphillis
|
|
Middle aged woman with optic neuritis
|
MS
|
|
Middle aged woman with ptosis
|
Myastenia Gravis
|
|
MS equivalent in child (10 yo)
|
Metachromatic Leukodystrophy
|
|
Middle aged man with descending paralysis
|
ALS
|
|
Asymmetrical paralysis weeks after gastroenetritis
|
Polio
|
|
Fasciculations in a neonate
|
Wednig Hoffman
|
|
Another name for Guillen Barre
|
Inflammatory Polyradiculoneuropathy
|
|
3 Neuromuscular Diseases with Fasciculations
|
Werdnig Hoffman
Polio ALS |
|
3 Neuromuscular Diseases that cause cerebral signs
|
Fredrick Ataxia
Ataxia Telangectasia Adrenal Leukodystrophy |
|
Fasciculations are a specific sign of what?
|
Lower motor neuron damage
|
|
Fasciculations in a newborn
|
Werdnig Hoffman
|
|
Fasciculations in a middle aged male
|
ALS
|
|
Fasciculations 2 wks after gastroenteritis
|
Polio
|
|
Clues for Ataxia Telangectasia
|
Cerebellar signs in 5 yo
Spider veins on skin IgA deficiency |
|
Clues for Friedrick's Ataxia
|
Cerebellar signs in 5 yo
Retinitis Pigmentosa Scoliosis |
|
Clues for adrenal leukodystrophy
|
Problem metabolizing long chain fatty acids
|
|
Definition of Cerebral Palsy
|
Permanent neurological damage suffered before age 21
|
|
Vasculitis 2 wks after common cold
|
Berger's
|
|
Smoking jew w/ necrotizing vasculitis
|
Buerger's
|
|
Vasculitis w/ family history of deafness and cataracts
|
Alports
|
|
Strawberry Tongue
|
Kawasaki's
|
|
Fibrin split products
|
DIC
|
|
Vasculitis 2 wks after E Coli Gastroenteritis
|
HUS
|
|
Vasculitis w/ fever, thrombocytopenia and neurological problems
|
Idiopathic Thrombocytopenia Purpura
|
|
Midsized artery vasculitis (particularly GI and Kidney)
|
Polyarteritis Nodosa
|
|
Vasculitis with sinus, lungs and kidney involvement
|
Waegner's Granulomatosis
|
|
Vasculitis w/ linear immunoflourescence on GBM w/ lung involvement
|
Goodpasture's
|
|
Vasculitis with pulmonary infiltrates w/ eosinophilia
|
Churg Strauss
|
|
Glomerulonephitis 2 wks post stre throat
|
Post Strep Glomerulonephritis
|
|
Glomerulonephritis 2 wks after a vaccination
|
Serum Sickness
|
|
Anti-cardiolipin, anti-sm, anti-ds dna antibodies
|
SLE
|
|
Septic Emboli
|
Subacute Bacterial Endocarditis
|
|
2 Muscle types least affected by neuromuscular disease. Why?
|
Smooth muscles and cardiac muscles because they have autonomics
|
|
How do you differentiate between myastenia gravis and myastenia syndrome?
|
MG gets weaker with contractions. Stronger with edrophonium test. Myastenic syndrome gets stronger with contractions and weaker with edrophonium test.
|
|
What is the defect in myastenic syndrome?
|
The sarcoplasmic reticulum is slow in sequestering Calcium leading to stronger muscle contractions.
|
|
Another name for myastenic syndrome
|
Eaton-Lambert syndrome
|
|
What cancers are associated with myastenic syndrome (Eaton-lambert)?
|
Small cell of the lung
|
|
What cancers are associated with Myastenia Gravis?
|
Thymoma
|
|
What cancers are associated with Dermatomyositis?
|
Visceral cancers (MC Colon Cancer)
|
|
Defect in Duchenne's Muscular Dystrophy?
|
Defect in the dystrophin protein
|
|
Early onset mutation
|
nonsense
|
|
Late onset mutation
|
missense
|
|
Mutation that makes a different protein
|
missense
|
|
Mutation that makes a stop codon?
|
nonsense
|
|
Purine to purine mutation
|
Transition
|
|
Purine to pyrimidine or vice versa mutation
|
Transversion
|
|
A myastenia gravis patient treated with Neostigmine presents with weakness, what is the course of action?
|
Determine if this is worsened myastenia gravis or cholinergic crisis due to Neostigmine. Repeate edrophonium test, if symptoms improve, increase neostigmine. If symptoms worsen, administer atropine and decrease the neostigmine dose.
|
|
What structures does Freidrick's Ataxia affect?
|
Dorsal colums and spinocerebellar pathway
|
|
What structure does adrenal leukodystrophy affect?
|
Cortex
|
|
CP that affects legs more than arms?
|
Spastic Diplegia (eg CMV)
|
|
CP which affects Basal Ganglia
|
Chorio Athetotic
|
|
CP where patient has no tone in body
|
Atonic
|
|
Infection that can cause spastic hemiplegia?
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CMV
|
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What can cause spastic hemiplegia
|
CMV, Stroke
|
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What can cause chorio athetotic CP?
|
Kernicterus
|
|
Only vasculitis with normal platelet count?
|
HSP
|
|
Only vasculitis with high platelet count?
|
Kawasaki
|
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Cause of death in all vasculitides is heart failure except which one? From what do they die?
|
Lupus: they die of Renal Failure
|
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Which protein is decreased in all vasculitides?
|
Haptoglobin
|
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What is the cellular response seen with all vasculitides?
|
T-Cells and Macrophages
|
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Clues for Adrenal Leukodystrophy
|
Babinski
Electrolyte Abnormality Problem metabolizing long chain fatty acids Adrenal Failure |
|
Mucositis, rash on palms and soles, Cervical lymph nodes, Temp >102 for >3 days
|
Kawasaki
|
|
Fever, Thrombocytopenia, Neurological Problems
|
TTP
|
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Vasculitis w/ Midsized arteries (GI and Renal) assoc w/ Hep B and P-ANCA.
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PAN
|
|
Allergic Vasculitis
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Churg-Strauss
|
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Cardiac infection caused by Strep Viridans (Vasculitis)
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Subacute Bacterial Endocarditis
|
|
Tram tracks w/ C3 nephritic factors in BM
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MPGN I
|
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Tram tracks with low complement (dense deposit disease)
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MPGN II
|
|
Mildest form of scleroderma, patchy involvement
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CREST
|
|
Anti-sm scl-70 and anti smooth muscle
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Scleroderma
|
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Scleroderma with organ involvement
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Progressive Systemic Sclerosis
|
|
Symmetrical polyarteritis, worse in AM, periosler erosion on Xray
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Rheumatic Arthritis
|
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Arthritis with iridesis
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Juvenile Rheumatoid Arthritis
|
|
RA + Leukopenia + splenomegaly
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Felty's
|
|
RA + GI ulcers
|
Behcets
|
|
RA + dry eyes, dry mouth
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Sjorgrens
|
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Vasculitis with GI bleeding, intussusception, normal platelet count
|
HSP
|
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Vasculitis whose most common cause is sepsis
|
DIC
|
|
MCC of renal failure in children
|
HUS
|
|
Vasculitis with which hep B is associated
|
PAN
|
|
Vasculitis that causes Pulmonary Infiltrate with Eosinophilia
|
Churg Strauss
|
|
Vasculitis with xeropthalmia, xerostomia
|
Sjorgren's
|
|
MCC of Arthritis in middle aged female
|
RA
|
|
Only arthritis that attacks the synovium
|
RA
|
|
S1 is made by
|
Closure of mitral and tricuspid valves
|
|
S2 is made by
|
Closure of aortic and pulmonic valves
|
|
s3 means
|
Volume overload
DIlation Decompensation |
|
s4 means
|
Pressure overload
Hypertrophy Compensation |
|
What produces an S2 Split?
|
Delayed closure of the pulmonic valve
|
|
Wide split S2 means
|
Increased oxygenation
Increased Ventricular volume Delayed pulmonary closure |
|
Narrow split S2 means
|
Decreased volume in the left ventricle
|
|
HOlosystolic Murmur
|
Mitral regurgitation
Tricuspid Regurgitation VSD |
|
Fixed S2 Split
|
ASD
|
|
Continuous Machine LIke Murmur
|
PDA
|
|
Mid systolic click
|
Mitral Prolapse
|
|
What is normal CVP?
|
3-5
|
|
What is normal PCV
|
12
|
|
What does the systolic component of blood pressure represent?
|
Pressure
|
|
What does the diastolic component of blood pressure represent?
|
Volume
|
|
Ejection clicks represent
|
Systolic murmurs
|
|
Opening snaps represent
|
Diastolic Murmurs
|
|
What factor produces murmurs?
|
Turbulence
|
|
Do right heart sounds get louder on inspiration or expiration?
|
Inspiration
|
|
Do left heart sounds get louder on expiration or inspiration?
|
Expiration
|
|
MCC Aortic Stenosis <30 yo
|
<30 Bicuspid Valve
|
|
MCC Aortic Regurgitation
|
Aging
Collagen Disease |
|
MCC Mitral Stenosis
|
Rheumatic Fever
|
|
MCC Mitral Regurgitaion
|
Mitral Valve Prolapse
Endocarditis Collagen Disease |
|
MCC Tricuspid Stenosis
|
Rheumatic Fever
Carcinoid |
|
MCC Tricuspid Regurgitation
|
Acute Endocarditis (MC: IV Drug Use)
|
|
MCC Pulmonary Stenosis and Pulmonary Regurgitation
|
Congenital Anomaly
|
|
Clues for Aortic Stenosis
|
Head bobbing
Quinke's Pulses Wide Pulse Pressure Waterhammer Pulse |
|
How can you accentuate Aortic Stenosis?
|
Lean fwd
Make a fist Blow up BP Cuff Squat |
|
How do you accentuate IHSS?
|
Valsalva
Stand Up |
|
Clues for IHSS
|
Athlete who passes out
Harsh systolic murmur Pulsus Biferiens Disorganized myofibrils on biopsy |
|
What causes IHSS?
|
The IV Septum is top heavy and falls into the ventricle preventing it from emptying during diastole
|
|
Diastolic blowing murmurs
|
Aortic Regurgitation
Pulmonic Regurgitation |
|
Diastolic rumbling murmurs
|
Mitral Stenosis
Tricuspid Stenosis |
|
Systolic Ejection Murmurs
|
Aortic Stenosis
Pulmonic Stenosis |
|
What are the two main types of effusions?
|
Transudate
Exudate |
|
Which type of effusion is mostly water and which type is mostly protein?
|
Transudate is mostly water
Exudate is mostly protein |
|
What are the main causes of a transudate?
|
Increased hydrostatic pressure
|
|
What two diseases cause increased body fluid and lead to a transudate?
|
CHF, Renal Failure
|
|
What 2 diseases cause decreased body fluid and lead to a transudate?
|
Cirrhosis
Nephrotic syndrome |
|
What is the main cause of an exudate?
|
Decreased oncotic pressure
|
|
What causes purulent exudates?
|
Bacterial infection
|
|
What causes granulomatous exudates?
|
Non-bacterial infections
|
|
What causes caseating exudates?
|
TB Infections
|
|
What causes Fibrinous Exudates?
|
Collagen Vascular Disease
Uremia TB |
|
What causes hemmorhagic exudate?
|
Trauma
Cancer |
|
MCC Restrictive Cardiomyopathy
|
Collagen Vascular Disease
Amyloidosis Hemochromatosis |
|
MCC Constrictive Cardiomyopathy
|
Tamponade
Cancer |
|
MC Congenital Heart Disease
|
VSD
ASD PDA Coarctation |
|
MC Cyanotic Heart Disease
|
Transposition of the great vessels
|
|
MC Cyanotic Heart disease >1 mo
|
Tetrology of Fallot
|
|
List 9 Cyanotic Heart Diseases
|
Transposition
Tetralogy Truncus Arteroisus Total anomolous venous return Tricuspid Atresia Pulmonary Atresia Aortic Atresia Hypoplastic Left Heart Epstein's Anomaly |
|
Clues for coarctation
|
Rib notching on XR
Differential Pulses Differential Cyanosis |
|
Clues for Tetrology of Fallot
|
I -IV Septal Defect
H- Hypertrophic L Heart O- Overriding Aorta P- Pulmonic Stenosis Blue while feeding, pink while crying. Child squats while playing. |
|
Clues for truncus arteriosus
|
Spiral Membrane did not develop
|
|
Clues for Epstein's Anomoly
|
Pregnant mom Rx with Lithium
Tricuspid valve develops in R ventricle |
|
CLues for total anomolous venous return
|
Snowman sign on X-Ray
|
|
What components of tetralogy of Fallot determines the prognosis
|
Degree of pulmonic stenosis
|
|
What two factors are used to determine whether fluid is transudate or exudate?
|
Protein <2g = Transudate
Specific Gravity < 1.012 = Transudate |