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Daily Flashcard Quizzes > 7/16 > Flashcards

7/16 Flashcards

1
Q

how do you calculate RBF and RPF

A

RBF = (PAH clearance) / (1-Hct)

RPF = (PAH clearance)

PAH clearance = [(urine PAH) x (urine flow)] / (plasma PAH)

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2
Q

how does the lecithin-sphingomyelin L/S ratio change in a developing baby

A

they’re ~the same until about 30 weeks, then L starts increasing while sphingomyelin stays roughly the same.
This increases the L/S ratio

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3
Q

how is glucose taken into the cells

A

facilitated diffusion via carrier-mediated transport

the GLUT carrier proteins are stereoselective for D-glucose

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4
Q

what is ferritin

A

an intracellular iron-binding storage protein

useful serum marker of total body iron stores

decreased in iron-deficiency anemia
elevated in iron-overload or infection

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5
Q

what is transferrin

A

molecule that delivers iron to liver and bone marrow

measure of iron in blood

for every 3 transferrin molecules, 1 will be bound to Fe.

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6
Q

what is TIBC and % saturation

A

TIBC:
measure of transferrin molecules in the blood

% saturation:
percentage of transferrin molecules that are bound by iron (normal is 33%)

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7
Q

what happens to Iron lab values when you have low iron

A

Low ferritin
(storage of Fe is depleated)

high TIBC
(always opposite of Ferritin)

low serum Fe

low % saturation

high Transferrin (when there’s low Ferrying, the liver will make more TF to try to increase Fe, and that’s also where the high TIBC comes from)

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8
Q

where is the majority of water reabsorbed in a nephron

A

proximal convoluted tubule

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9
Q

what is the thin descending loop known as

A

concentrating segment
passively reabsorbs water.
impermeable to Na+

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10
Q

what happens in the thick ascending loop

A

Na/K/2Cl transporter to reabsorb some of these ions.
urine becomes less concentrated as it ascends

impermeable to water, so it stays in the tubules.

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11
Q

what happens in the early Proximal convoluted tubule

A

reabsorbs >60% water filtered by glomerulus, regardless of hydration status

reabsorbs all glucose and amino acids

reabsorbs most small ions and uric acid

isotonic absorpption

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12
Q

what happens in the early distal convoluted tubule

A

makes urine fully dilute by reabsorbing Na and Cl.

urine is at its lowest osmolality here

H2O is impermeable in the early portion. becomes variable later on with Vasopressin

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13
Q

what is Hepatitis B’s replication sequence

A

dsDNA –> (+)RNA template –> dsDNA

HBV replicates via reverse transcriptase, even though it is a DNA virus

it occasionally goes to a single strand mode

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14
Q

what is the only ssDNA virus

A

Parvovirus B19

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15
Q

what is the histologic progression of an ischemic stroke

A 
12-48 hrs:
Red neurons (eosinophils! and loos of Nissl substance!!)

1-3 days:
necrosis + neutrophils

3-7 days:
macrophage/microglia and myelin phagocytosis

1-2 weeks:
reactive gloss and vascular proliferation
(liquefactive necrosis)

> 2 weeks:
glial scar formation w/ astrocytes

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16
Q

Run through Aortic/Pharyngeal arch derivatives

A

1st:
maxillary artery
CN 5
“1st is maximal”

2nd:
stapedial artery and hypoid artery
CN 7
“Second = Stapedial”

3rd:
Common Carotid artery and proximal internal Carotid
CN 9
“C is 3rd letter”

4th:
on left, aortic arch
on right, proximal R subclavian artery
CN 10
"4th arch = 4 limbs = systemic"

6th:
proximal pulmonary arteries and (L) ductus arteriosus
CN 10
“6ulmonary arch”

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17
Q

run through pharyngeal pouch derivatives

A

1st:
ears

2nd:
tonsils

3rd:
inferior parathyroid
thymus

4th:
superior parathyroid
parafollicular C cells of thyroid

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18
Q

what stimulates neutrophil migration to inflammation

A

Leukotriene B4

“Neutrophils arrive B4 others”

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19
Q

what does PGI2 do

A

PGI2 inhibits platelet aggregation and promotes vasodilation

“Platelet gathering Inhibitor”

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20
Q

what does complement do

A

they’re inflammatory anaphylotoxins that trigger histamine release from mast cells

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21
Q

what does interferon-gamma do

A

activates macrophages, increases MHC expression, and promotes Th1 cell differentiation

produced primarily by activated T cells and NK cells

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22
Q

what does Thromboxane A2 do

A

increases platelet aggregation and vasoconstriction

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23
Q

what are the 3 important chemotactic agents

A

LTB4
C5a
IL-8 (clean up on aisle 8)

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24
Q

what does hydroxyurea do

A

increases HbF synthesis

reserved for sickle cell pts with frequent pain crises

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25
Q

what is the defect in xeroderma pigmentosum

A

NER, a defect in an ENDONUCLEASE

pts have increased sensitivity to UV light and cannot repair pyrimidine dimers

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26
Q

what is caused by a defect in DNA mismatch repair

A

HNPCC or Lynch syndrome

high incidence of colorectal, endometrial, and ovarian cancer (CEOs)

this is EXONUCLEASE proofreading defects

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27
Q

what do Ras mutations cause

A

commonly pancreatic or colorectal cancer

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28
Q

what do p53 mutations cause

A

Li-Fraumeni syndrome (wide range of malignancies at a young age)

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29
Q

what is Fanconi anemia

A

mutations in genes responsible for repairing DNA crosslinks

causes:
aplastic anemia
short stature
ABSENT THUMBS
increased malignancy risk
PCT defect, where everything is excreted
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30
Q

what is gold standard for detecting a microdeletion

A

FISH

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31
Q

what does DiGeorge present with

A

micro deletion!!!
CATCH22

cleft lip/palate/UVULA
Abnormal facies
Thymic aplasia
Cardiac abnormalities
Hypocalcemia/hypo-PTH

22q11.2 microdeletion

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32
Q

what defect causes the most common heme synthesis disorder

A

defect in uroporphyrinogen decarboxylase

causes porphyria cutanea tarda, manifesting as photosensitivity with blisters!!

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33
Q

what are the stop codons

A

UAA
UAG
UGA

“you are annoying
you are gross
you go away”

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34
Q

what is the Duchenne pathogenesis

A

frameshift or nonsense mutation –> truncated dystrophin

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35
Q

what does dystrophin do

A

dystrophin is supposed to help anchor muscle fibers

connect the intracellular cytoskeleton to the transmembrane proteins and EC matrix

mutated in Duchenne

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36
Q

what is a nonsense mutation

A

premature stop codon

“stop the nonsense”

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37
Q

what is a missense mutation

A

nucleotide substitution that changes the amino acid

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38
Q

what does acute mitral regurg cause

A

high LA pressures and pulmonary edema

increased LV preload

decreased LV after load (the regurg pathway back to the LA helps remove some LV blood during systole)

overall increased Ejection fraction
(increased preload + decreased afterload)
however, much of that total SV is lost back to the LA,
causing a decreased forward SV and reduced CO (hypotension)

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39
Q

what is eccentric hypertrophy

A

dilated cardiomyopathy

volume overload

2/2 aortic regurg

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40
Q

what is concentric hypertrophy

A

hypertrophic cardiomyopathy

LV is having to pump against a stiff aortic valve (aortic stenosis)

41
Q

when you hear S3 vs S4 heart sounds

A

S3:
dilated cardiomyopathy
blood is entering a huge space, so it “plops” in

S4:
hypertrophic cardiomyopathy
blood is being forced into the small (muscular) ventricle, so it the atrial does one last “kick” to fill it the rest of the way

42
Q

how does hypovolemia affect RPF, GFR, and FF

A

very reduced RPF
reduced GFR)

this leads to compensatory efferent arteriole vasoconstriction via RAS (and afferent dilation) which
raises the FF and maintains GFR at near normal

increase in FF
(FF = GFR/RPF)

as RPF contines to decline, increasing the glomerular oncotic pressure will eventually overwhelm the compensatory increase in hydrostatic pressure, leading to a quick drop in GFR and renal failure

43
Q

what is poison ivy

A

type of contact dermatitis,
a delayed-type hypersensitivity

TYPE 4 HYPERSENSITIVITY

T-CELL MEDIATED

44
Q

What are the 2 phases of a delayed type hypersensitivity

A

type 4:

1:
sensitization phase
creation of hapten-specific T cells
takes 10-14 days
cutaneous dendritic cells take up the haptens and express them on MHC class 1 and 2 molecules as happen-conjugated peptides.
these dendritic cells travel to the draining LNs and interact w/ happen-sensitive CD4 and CD8 T cells, causing activation and clonal expansion

2:
elicitation phase
occurs within 2-3 days following re-exposure to the same antigen (or after 1st exposure to something highly antigenic like urushiol/poison ivy)
the hapten is taken up by skin cells and causes activation of hapten-sensitized T cells in the dermis/epidermis.
causes inflammatory response and clinical manifestations of contact dermatitis

45
Q

what does primary (psychogenic) polydipsia present with labs

A

hyponatremia with a low initial urine osmolality

a water deprivation study will differentiate between Primary Polydipsia and DI.

46
Q

how does a water deprivation test work

A

pt not allowed to drink
measure urine osmolality

then administer vasopressin (ADH)
and re-check urine

Primary polydipsia:
pts will concentrate urine during water deprivation (appropriate response)
ADH admin does not significantly change urine concentration because the pt has already appropriately concentrated urine themselves

DI:
inability to concentrate urine
2/2 either low ADH (central DI) or decreased renal response to ADH (nephrogenic DI)
plasma Na will be high (losing dilute water)
water deprivation will not lead to a significant change in osmolality

47
Q

how do you treat central DI

A

desmopressin (synthetic ADH)

48
Q

how do you treat nephrogenic DI

A

thiazide diuretics
(to induce mild hypovolemia, increasing proximal tubule Na and water reabsorption)

or indomethacin 
(decreases prostaglandin synthesis, which inhibit ADH)
49
Q

what are sclerotic bone lesions

A

osteoblastic

think prostate cancer

50
Q

what type of bone manifestation is found in multiple myeloma

A

osteolytic lesions (lucent)

51
Q

what drug can cause priapism

A

trazodone

52
Q

how do schwannomas present

A

biphasic pattern of cells
S-100 positivity (neural crest origin)

commonly with acoustic neuromas with CN8

53
Q

what is a C1 esterase inhibitor deficiency

A

causes hereditary angioedema due to unregulated activation of kvllikrein –> bradykinin (potent vasodilator associated w/ angioedema)

ACE inhibitors are contraindicated

C1 esterase inhibitor normally prevents excessive cleaving of C2 and C4

54
Q

what does a DIC peripheral smear show

A

schistocytes and thrombocytopenia

decreased fibrinogen

prolonged PT, PTT

elevated D-dimer

55
Q

how do competitive inhibitors work

A

compete with substrate for active binding sites of enzymes

add more substrate to achieve the same rxn rate (increases Km- shifts the curve to the right)

enzyme function is not changed, so maximal velocity is unchanged

56
Q

what do noncompetitive inhibitors do

A

most bind allosteric sites, resulting in conformational change that decreases activity and slows rxn rate (decreases Vmax- shifts curve down)

they don’t change Km and cannot be overcome with higher substrate concentrations

57
Q

what is a renal tumor composed of vessels, smooth muscle, and fat

A

angiomyolipoma

58
Q

what are angiomyolipomas associated with

A

they’re renal tumors associated with tuberous sclerosis

59
Q

what is tuberous sclerosis

A 
Hamartomas in CNS and skin
Angiofibromas
Mitral regurgitation
Ash-leaf spots
cardiac Rhabdomyosarcoma (tuberous sclerosis)
auto dOminant
Mental retardation
renal Angiomyolipomas
Seizures
Shagreen patches

“HAMARTOMAS”

60
Q

what is the Rathke pouch from embryogenically

A

oral ectoderm

61
Q

what comes from ectoderm

A

surface ectoderm:
lots of external “attract-o-derm” structures
Rathke pouch

neuroectoderm:
brain/CNS

neural crest:
PNS and nearby non-neural structures

62
Q

what comes form mesoderm and endoderm

A

Endoderm:
gut tube-derivatives and internal organs EXCEPT SPLEEN

Mesoderm:
SPLEEN
“means of living”
muscle, bone, cartilage, etc

63
Q

what is the most common acute compartment syndrome injury in the leg

A

deep peroneal (fibular) nerve

also includes anterior tibial artery

64
Q

what does total peripheral resistance and heart contraction velocity look like when you’re in hypovolemia

A

both are high due to sympathetic activation

fluid administration will reduce sympathetic activation and decrease both of these

65
Q

what is oseltamivir’s MOA

A

neuraminidase inhibitor

decreases release of virion particles

66
Q

what does oseltamivir treat

A

Influenza A and B viruses

67
Q

what do you see delta waves in

A

Wolf-Parkinson White syndrome

68
Q

what is wolf parkinson white syndroem

A

accessory pathway that bypasses the AV node and directly connects the atria and ventricles

69
Q

what is the prominent artery and often spared artery in polyarteritis nodosa

A

prominent:
renal artery

spared:
pulmonary

70
Q

what is a common cause of osteomyelitis in sickle cell pts

A

salmonella

also staph, so you should pick abx to cover both

71
Q

what is salmonella’s main virulence factor

A

special capsule called “Vi antigen” that prevents it from opsonization and phagocytosis

72
Q

how are particles cleared in the alveoli

A

phagocytosis from alveolar macrophages

mucociliary transport is used in bronchi and proximal bronchioles

73
Q

what is tennis elbow

A

lateral epicondylitis

repetitive wrist extension, giving you pain on lateral elbow

74
Q

what is special about Herpes meningitis

A

particular affinity for temporal lobe,

causing personality changes and receptive aphasia (Wernicke’s aphasia), cranial nerve palsies, and seizures

75
Q

which two antibiotics bind directly to transpeptidases

A

penicillin and cephalosporins

76
Q

what are transpeptidases

A

penicillin-binding proteins

they function to build the bacteria cell walls

77
Q

what does vancomycin bind to

A

cell wall glycoproteins, which prevents transpeptidases from forming cross-links

78
Q

what is deposited in PSGN

A

immune complex of IgG, IgM, and C3

this gives you “spike and dome”

79
Q

what gives you spike and dome renal biopsies

A

PSGN and immune complex deposition of IgG, IgM, and C3

80
Q

when do you see renal fibrin deposition

A

RPGN

81
Q

what does chronic graft rejection look like

A

obliterative intimal thickening, (renal) tubular atrophy, and interstitial fibrosis

82
Q

where do fish toxins bind

A

voltage-gated Na channels

83
Q

what’s the pathogenesis of MS

A

T cell and antibody-mediated response against the CNS- oligodendrocytes and myelin

84
Q

what are the 2 uncommon ways to inherit Down Syndrome

A

unbalanced Robertsonian translocation
(extra genetic material from Chr 21 attached to another chromosome)

mosaicism:
2 distinct cell lines as a result of nondisjunction during mitosis (one nl genotype, one with trisomy 21)
proportion determines severity of Down

85
Q

what does Hepatitis B histology look like

A

finely granular, pale pink/eosinophilic, ground-glass appearance

granular eosinophilic “ground glass” or “sand nuclei” appearance

86
Q

what does Hepatitis C histology look like

A

lymphoid aggregates w/ focal areas of macrovascular steatosis

87
Q

what does Hepatitis A histology look like

A

hepatocyte swelling, monocyte infiltration, and

Apoptotic Councilman bodies!

88
Q

what does hepatic steatosis and later, alcoholic hepatitis look like on histology

A

macrovascular fatty change (triglyceride accumulation)

alcoholic hepatits:
swollen and necrotic hepatocytes with neutrophilic infiltration
MALLORY BODIES (intracytoplasmic eosinophilic inclusions of damaged keratin filaments)

89
Q

what does alcoholic cirrhosis biopsy look like

A

micro nodular, irregularly shrunken liver w/ “hobnail” appearance

sclerosis around central vein (zone 3)

90
Q

what happens if you have Hemoglobin that has an increased affinity for oxygen

A

you reduce its ability to reduce oxygen in the peripheral tissues

this means your kidneys will see lower oxygen levels, and cause compensatory erythrocytosis

91
Q

how can PID cause infertility

A

inadequate Antibiotic treatment (too short or not enough coverage), leading to fallopian tube scarring, which can turn into infertility

92
Q

describe scarlet fever

A

blanching, sandpaper-like body rash
strawberry tongue!
circumoral pallor
possible gray-white exudates

in the setting of group A strep pharyngitis

can predispose you to rheumatic fever and PSGN

93
Q

what does TB’s cord factor do

A

inactivates neutrophils, damages mitochondria, and induces release of TNF

grows as “serpentine” cords

94
Q

how is anthrax typically acquired

A

occupational hazard

those who handle livestock that have not been immunized or those who handle hides

95
Q

what is the progression of alcohol withdrawal

A

6-24 hrs:
anxiety, insomnia, tremor, diaphoresis, palps, GI upset, intact orientation

12-48 hrs:
seizures

12-28 hrs:
hallucinations ; intact orientation

48-96hrs:
delirium tremens:
confusion, agitation, fever, tachy, HTN, diaphoresis, hallucinations

96
Q

why can you not use daptomycin in pneumonia

A

inactivated by surfactant

97
Q

major side effect of daptomycin

A

myopathy

monitor with CPK level

98
Q

what’s a common cause of aspiration pneumonia

A

bacteroides fragilis

“bacteroides in the back of your mouth”

99
Q

what’s a common saying to remember how to use clindamycin and metronidazole

A

“clindamycin above the diaphragm, metronidazole below the diaphragm”

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