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1
Q

Stellate Cells

A

Perisunusoidal cells (pericytes) that secrete TGF-beta and are responsible for the disruption of the liver architecture in cirrhosis

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2
Q

Reye syndrome mechanism

A

Aspirin metabolites decrease beta oxidation by reversible inhibition of mitochondrial enzymes

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3
Q

Emphysema (centri vs panacinar) location predominance

A

Centriacinar (tobacco) - upper lobes, Panacinar (a1at) - lower lobes

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4
Q

Tx for Crigler-Najjar Type II (less severe)

A

Phenobarbital – induces liver enzyme synthesis

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5
Q

Epinephrine metabolites within lysosomes?

A

Dubin-Johnson syndrome

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6
Q

Wilsons disease causing blood issues?

A

Yes – hemolytic anemia

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7
Q

p-ANCA

A

UC, Churg-Strauss, PSC, Microscopic polyangitis, RA, occasionally polyarteritis nodosa

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8
Q

Metanephric mesenchyme

A

Glomerulus to DCT

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9
Q

Ureteric bud

A

Collecting system (including collecting ducts)

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10
Q

Hartnup disease

A

Cant reabsorb NEUTRAL amino acids in PCT –> includes tryptophan. Tx with high protein diet + niacin

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11
Q

Syndrome of apparent mineralocorticoid excess

A

Hereditary deficiency in 11B-hydroxysteroid dehydrogenase –> increased cortisol (since its not being convereted into cortisone). Can acquire from glycyrrhetic acid which is present in licorice since it blocks the activity of the enzyme

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12
Q

EPO release location

A

Interstitial cells in peritubular capillary bed

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13
Q

1,25-(OH)2D3 synthesis location

A

PCT cells via 1-a-hydroxlase

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14
Q

Renal oncocytoma

A

Benign EPITHELIAL cell tumor w/large eosinophilic cells + abundant mitochondria, but no perinculear clearing. ddx for renal cell, similar presentation

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15
Q

Thyroidization of the kidney + eosinophilic casts

A

Chronic pyelonephritis

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16
Q

Renal papillary necrosis causes

A

Sickle cell (trait or disease), acute pyelo, analgesics, diabetes

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17
Q

Ethacrynic acid

A

Loop diuretic similar to furosemide, but can be used in patients with sulfa allergies. but be careful because can cause hyperuricemia (contraindicated in gout)

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18
Q

Triameterene and amiloride

A

K sparing diuretics without the benefit of alodsterone antagonism (heart failure survival)

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19
Q

Aliskiren

A

Direct renin inhibitor

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20
Q

Pralidoxime

A

AKA 2-PAM, regenerates AChE if given early

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21
Q

Cold feels hot, hot feels cold + cholinergic poisoning symptoms

A

Ciguatoxin (raw reef fish consumption)

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22
Q

Anyphlaxis after eating dark-meat fish

A

give antihistamines because the bacterial histidine decarboxylase is converting histidine to histamine so it looks like an allergy

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23
Q

DNA methylation

A

Occurs at CpG islands, but on cytosine and adenine residues

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24
Q

Random molecular facts

A
  • Thiamine has a methyl - Demaminate cytosine to make uracil - Need Glycine, aspartate, glutamine to make purines (GAG)
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25
Q

Immunosupressives in de novo pyrimidine and purine synthesis

A
  • Leflunomide inhibits dihydroorotate dehydrogenase (carbamoyl phosphate to orotic acid) - Mycophenolate and ribavirin inhibits IMP dehydrogenase (IMP to GMP) - Hydroxurea inhibits ribonucleotide reductase (UDP to dUDP) - 6MP, AZA inhibit PRPP to IMP - 5FU inhibits thymidylate synthase (dUMP to dTMP) - MTX/TMP/pyrimethamine inhibits dihydroflorate reductase (dUMP to dTMP cofactor)
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26
Q

Adenosine deaminase deficiency

A

Backup of ATP and dATP inhibits ribonucleotide reductase which inhibits DNA synthesis. Thus ADA deficiency (SCID) is like being born with hydroxyurea

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27
Q

Probenecid

A

Increases uric acid excretion in urine

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28
Q

Timing of DNA repair/example of disease

A

Nucleotide excision repair - G1 [xeroderma picmentosum] Base excision repair - throughout cell cycle Mismatch repair - G2 [HNPCC] Nonhomologous end joining [Ataxia teleangiectasia, Fanconi anemia]

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29
Q

Osteogenesis imperfecta mechanism

A

Cant form triple helix pro-alpha chains in RER

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30
Q

Ehlers Danlos and Menkes disease mechanism

A

Problems with post-exocytosis cross linking to make collage fibrils

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31
Q

Ehlers Danlos types

A

Classic is collagen type V, vascular is collagen type III

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32
Q

Menkes mechanism more specific

A

X-recessive. Impaired copper absorption/transport b/c of defective menkes protein –> decreased acticity of lysyl oxidase since copper is a cofactor –> problems with making colagen fibrils since that protein is needed for the covalent cross linking

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33
Q

Marfan mechanism

A

Defect in fibrillin which is scaffolding for tropoelastin (forms a sheath around elastin)

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34
Q

Shortcut rules for AD and AR

A

AD - defects in structural genes AR - enzyme deficiencies

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35
Q

Hereditary hemorrhagic telangiectasia (aka Osler-Weber-Rendu syndrome)

A

Disorder of blood vessels: Telangiectasia, recurrent epistaxis, skin discolaration, AVMs, GI bleeding, hematuria [think Leigh in terms of skin and nose bleeds]

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36
Q

Cystic fibrosis metabolic effects

A

Like taking a loop diuretic (contraction alkolosis and hypokalemia)

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37
Q

Duchenne vs Becker genetics

A

Both XR. Frameshift vs nonframeshift (truncated/deletion vs partially functional). Deletions can cause both. Duchenne can also be duplicationsand nonsense)

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38
Q

Myotonic type 1

A

AD. My ticker, my toupe, my testicles, my tonia

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39
Q

Robertsonian translocation locations

A

13-15, 21-22

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40
Q

Vit A

A

Function: Epithelial differentiation into specialized tissue, prevent squam metaplasia, treat AML (M3) and measles, visual pigment Deficiency: Night blindness, corneal degen, spots on conjunctiva, immunosupression Excess: Hepatic toxicity (guy who eats a liver and gets cirrhotic), pseudotumor cerebri

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41
Q

Vit B1 (thiamine)

A

Function: aTP (alpha ketogluturate, transketolase, pyruvate dehydrogenase) + branched chain ketoacid dehydrogenase Deficiency: Diagnose with RBC transketolase levels elevated. Impaired glucose breakdown.

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42
Q

Vit B2 (riboflavin)

A

Function: FAD/FMN, redox reactions (dehydrogenase) Deficiency: Cheilosis, corneal vascularization

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43
Q

Vit B3 (Niacin)

A

Function: NAD+, NADP+, redox reactions (dehydrogenase), derived from tryptophan and needs B2 and B6 for synthesis. Deficiency: Glossitis, pellegra Excess: Facial flushing (prostglandin excess), hyperglycemia (insulin resistance), hyperuricemia (caution in gout), hepatitis

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44
Q

Vit B5 (Pantothenic acid)

A

Function: CoA component, fatty acid synthase Deficiency: Dermatitis, enteritis, alopecia, adrenal insufficiency –> need for steroids and cholesterol

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45
Q

Vit B6 (pyridoxal)

A

Function: Transamination, decarboxlayion, glycogen phosphorylase. Hella neurotransmitters (SEND GABA) Deficiency: Convulsions, hyperirritability, periphernal neuropathy, sideroblastic anemias, subderm

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46
Q

Vit B7 (Biotin)

A

Function: Carboxylation (1 carbon additions). PO, AM, PM Deficiency: Rare. Dermatitis, alopecia, enteritis. excessive raw egg whites or abx use.

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47
Q

B12 very basic function

A

Methylmalonyl CoA to Succinyl CoA (which furhter goes on to make heme) Homocysteine to methionine Deficiency results in homocysteine + methylmalonic acid levels

48
Q

B6 very basic function

A

Succinyl CoA to Heme Homocystein to cysteine Deficiency results in homocysteine levels

49
Q

Vit C

A

Function: necessary for dopamine B-hydroxylase to convert dopamine to NE. Reduce iron Deficiency: Scurvy Excess: N/V/D. Stones

50
Q

Vit E

A

Function: Antioxidant, protects RBC membrane from free radical damage Deficiency: Hemolytic anemia, acanthocytosis, posterior/spinocerbellar tract demylenation (resemlbes fredrieches ataxia, or B12 deficiency w/o megaloblastic anemia)

51
Q

Alcohol metabolism locations

A

Cytosol: EtOH –> acetaldeyde Microsome: P450 metabolism Mitochondria: Acetaldehyde –> Acetate

52
Q

Metabolism site shortcut

A

Synthesis in cytoplasm Degradation in mitochondria Both involved in urea cycle, gluconeogenesis, heme synthesis

53
Q

Arsenic’s 2 actions

A

1) causes glycolysis to produce zero net ATP 2) Inhibits lipoic acid (a necessary component of the pyruvate dehydrogenase complex)

54
Q

ATP producing steps in glycolysis

A

1) PEP to Pyruvate 2) 1,3PG to 3PG

55
Q

Activators of pyruvate dehydrogenase complex

A

ADP, Calcium, high NAD+/NADH ratio

56
Q

Pyruvate dehydrogenase complex deficiency

A

Build up of pyruvate –> neorologic defects + lactic acidosis + high serum alanine (because pyruvate gets shunted to lactate and alanine) Treat with ketogenic nutrients (lysine/leucine/high fat diet)

57
Q

What can pyruvate become? (4 things)

A

1) Alanine (via ALT) [B6 needs Biotin] replenish TCA or use for gluconeogenesis 4) Acetyl-CoA [B1, B2, B3, B5, Lipoic acid] If B3 involved, you’ll get NADH out of it (so Lactate, and acetyl-CoA)

58
Q

When do you get NADH in a reaction?

A

If B3 (Niacin) is a necessary cofactor for it

59
Q

Electronic transport chain summary

A

-Protons enter via: Complex I, III, IV. -Protons exit via: Complex V -NADH pairs with Complex 1 -FADH2 pairs with Complex 2 (Succinate dehydrogenase, the only enzyme that participates in both ETC and TCA) -CoQ between II and III, Cytochrome C between III and IV - Cyanide and CO block Complex IV

60
Q

ATP equivalents for NADH/FADH via ATP synthase

A

NADH = 2.5 ATP FADH = 1.5 ATP

61
Q

ETC poisonin

A

Oligomycin: Directly inhibits ATP synthase Aspirin: Uncoupling agent Thermogenin: Uncoupling agent in brown fat

62
Q

Gluconeogensis and fat

A

Odd chain fatty acids –> propionyl-CoA –> can enter TCA to become glucose Even chain fatty acids –> only yield Acetyl-CoA–> cannot ever become glucose

63
Q

NADPH uses

A

Fatty acid/cholesterol synthesis, glutathione reduction. Therefor it will be found in places that need it: lactating mammary glands, liver, adrenal cortex, sites of fatty acid or steroid synthesis, RBCs

64
Q

Disacharides

A

Lactose = galactose + glucose Sucrose = fructose + glucose Maltose = glucose x 2

65
Q

Galactokinase deficiency

A

Failure to develop a smile or track objects, infantile catarcts (galactitol via aldose reductase). Imagine a kid who doesn’t like to drink milk.

66
Q

Classic galactosemia

A

Failure to thrive, cataracts, hepatomegaly. E. coli sepsis in neonates. (galactose 1 phosphate) uridyltransferase

67
Q

Tissues that have BOTH aldose reductase (glucose to sorbital) AND sorbitol dehydrogenase (sorbitol to fructose)

A

Liver, ovaries, seminal vesicles. Need NADPH for aldose reductase and NAD+ for sorbitol dehydrogenase

68
Q

Tissues that have only or primarily aldose reductase

A

Schwann cells, retina, kidneys, lens (all places that get damaged with diabetics)

69
Q

Urea cycle

A

-Urea nitrogens are from NH3 and aspartate -Ordinarily, careless crappers are also frivilous about urinating

70
Q

Transporting ammonia via alanine and glutamate (general principles)

A
  • AA becomes an alpha-ketoacid once it donates its NH3 to an acceptor (alpha-ketogluturate) to form glutamate - Pyruvate + glutamate = Alanine - Alanine can go from muscle to liver where the NH3 is taken away to form glutamate with alpha-ketoglurate. Then glutamate can be turned into urea - Lactate returns from muscle to liver where it is converted to pyruvate, then to glucose, so it can go back
71
Q

Hyperammonemia pathophys

A

Will deplete alpha-ketoglutarate thus inhibiting TCA. Tx: lactulose to acidify, rifaximin to decrease colonic ammongiagenic bacteria, benzoate/phenylbutyrate to bind AAs to excrete them. Example of cause: liver disease, N-acetylglutamate synthase deficiency

72
Q

Ornithine transcarbamylase deficiency

A

XR, other urea cycle defects are AR. Body cant eliminate ammonia. Carbamoly phosphate converted to orotic acid (pyrmidine synthesis pathway) instead. no megaloblastic anemia like orotic aciduria

73
Q

PKU

A

-Low phenylalanine hydroxlase OR low tetrahydrobiopterin cofactor aka BH4 (malignant PKU) -Tyrosine now is essentially since it cant be synthesized from phenylalanine - Excess phenylaline will downregulate tyrosinase which converts tyrosine to melanin –> fair pigmented skin ALBINO Must body odor. Aspartame has phenylalanine

74
Q

Maple syrup urine disease

A

Branched chain amino acids dont get degraded because of low alpha-ketoacid dehydrogenase. B1 dependent enzyme, so supplement with thiamine

75
Q

Alkaptonuria

A

Tyrosine to fumurate pathway compromised because of homogentisate oxidase. Pigmented, arthralgias. Urine turnks black in air.

76
Q

3 causes of homocysteinuria (clinical manifestations: intellectual disability, marfinoid habitus, kyphosis, thrombosis, lens subluxation)

A

1) B12 deficiency: necessary coenzyme for homocystein methyltransferase to make methionine (tx: methionine in diet) 2) Cystationine synthase deficiency (tx: decrease methionine since that pathway will be predominant, increase cysteine since its missing now) 3) Decreased affinity of cystationine synthase for B6 (tx: increase B6 and cysteine in diet)

77
Q

Stimulators of glycogen phosphorylase kinase (which goes on to phosphorylate glyogen phosphorylase and promote gluconeogenesis)

A

PKA (via glucagon and B-receptor) Calcium-calmodulin during muscle contraction Calcium directly

78
Q

Glycogen storage disease summary

A

Von Gierke (T1): glucose 6 phosphate is only in liver, so hepatomegaly and a lot of glycogen in liver. High blood lactate level Pompe (T2): Lysosomal a14 glucosidase (acid maltase) defect trashing the pumps (hypertrophic cardiomyopathy, cardiomegaly, liver, muscle Cori (T3): 1,6 debrancher, gluconeogenesis is intact, mild form of Von Gierke but w/normal blood lactate level McArdle (T5): skeletal muscle gylocgen phosphorylase, so painful muscle cramps and myoglobinuria with exercise. Normal blood glucose levels. Tx with B6.

79
Q

Lysosomal storage disease high yield

A

Fabry disease: XR. Angiokeratomas, peripheral neuropathy. “Within the Fabric of the universe is a galaxy of skin spots” Gaucher disease: Hepatosplenomegaly. Pancytopenia. Crumpled tissue paper (lipid laden macrophages). Bone problems. “My BRO has an iPhone 3G (GlucocerBROsidase, GlucocereBROside) Niemann-Pick disease: Neurodegen. Hepatosplenomegaly. “No man picks his nose with his shpinger”. Foam cells (lipid laden macrophages). Cherry-red macula Tay-SaX disease: Neurodegen. Onion skin lysosomes. NO hepatosplenomegaly. Cherry-red macula. HeXo A, GM2 gang Krabbe disease: Peripheral neuropathy, optic atrophy. glboid cells (“glob of fat” Metachromatic leukodystrophy disease: Central + peripheral demyelination w/ataxia + dementia Hurler syndrome:Gargoylism, corneal clouding, hepatosplenomegaly. Heparan sulfate, dermatan sulfate. Hunter syndrome: XR. Mild Hurler + aggressive behavior (being a hunter) w/o corneal clouding. Heparan sulfate, dermatan sulfate.

80
Q

Fatty acid metabolism

A

Citrate shuttle (sytrate, synthesis), occurs in cytosol Carnitine shuttle (carnage), occurs in mitochondria Systemic primary carnitine deficiency leads to toxic accumulation of fatty acids outside in cyotosol: hypoketotic hypoglycemia. Similar presentation to medium chain acyl-CoA dehydrogenase deficiency, which results in the same presentation w/minor illness or fasting.

81
Q

Ketone bodies

A

Prolonged starvation –> decrease in oxaloacetate for gluconeogenesis –> buildup of acetyl-CoA –> shunts glucose/FFA towards production of ketone bodies Test only picks up acetoacetate (not B-hydroxbutyrate) RBCs cant use ketones

82
Q

Lipid metabolism

A

ApoE (in blood) = signal for liver takeup Apo CII (in blood) = cofactor/signal for lipoproteim lipase ApoB-48 (in lymph) = chylomicron ApoB-100 = 100% came from the liver. Also a marker for LDL uptake by tissue, binds LDL receptors. AI activates LCAT, only on chylomicron and HDL

83
Q

RR vs OR

A

Relative risk reports risk of developing disease in groups with or without exposure Odds ratio is for case-control because these patients already have the disease and we are looking at how their exposure in the past correlates.

84
Q

Platelet granules/endothelial

A

Dense granule = ADP, Ca2+ Alpha granule = vWF, fibrinogen Weibel-Palade bodies (endothelial cells) = vWF, P-selection Endothelial cells also have VIII

85
Q

Basophilia

A

CML

86
Q

Basophilic stippling in lead poisoning

A

From inhibition of rRNA degradation, aggregates of rRNA Also look for lead lines on gingivae and metaphyses of long bones Wirst and foot drop

87
Q

Eculizumab

A

Terminal complement inhibitor for paroxysmal nocturnal hemoglobinuria Pronounce “eludumab” to elude the immune system

88
Q

Corticosteroids on neutrophils and eos

A

Neutrophilia, but eosinopenia b/c squesters them in lymph nodes and cause apoptosis of lymphocytes

89
Q

Enzyme defects in porphyrias

A

Sideroblastic: ALA synthase (B6) Lead Poisoning: ALA dehydratase, Ferrochelatase Acute intermittent porphyria: Porphobilinogen deaminase Porphyria cutanea tarda: Uroporphyrinogen decarboxylase

90
Q

Pathophys of ITP

A

Antibodies against GpIIb/IIIa

91
Q

Pathophys of TTP

A

Inhibition or deficiency of ADAMTS 13 (vWF metalloprotease)

92
Q

Antithrombin deficiency effect on PT/PTT/bleeding time

A

None, could be trick question, be careful

93
Q

Reed-Sternberg Cells

A

CD15+, CD30+ (think biphasic, 15 yr olds and 30 yr olds)

94
Q

DDx for lytic bone lesion and hypercalcemia

A

Primary hyperparathyroidism (causes osteitis fibrosa cystica), multiple myeloma, Adult T-cell lymphoma

95
Q

Cerebriform nuclei

A

Mycosis fungoides/Sezary syndrome

96
Q

ALL

A

TdT+ and CD10+ if pre-B cell Can spread to testes/CNS

97
Q

SLL/CLL

A

CD20+ CD5+ Smude cells Autoimmune hemolytic anemia

98
Q

Hairy cell leukemia

A

TRAP+ Cells get TRAPed in red pulp, marrow fibrosis, get dry bone marrow Mature B-cells Tx with cladribine, pentostatin

99
Q

AML

A

Peroxidase+ M3 has cytoplasmic inclusions Risk factors with alkylating agents, radiation, myeloproliferative disorders

100
Q

CML

A

Low ALP (to contrast to leukomoid reaction) Basophilia Splenomegaly Can trasnform to AML or ALL (blast crisis) Tx with imatinib

101
Q

Langerhans cell histiocytosis

A

lytic bone lesions, skin rash, reucrrent otitis media, mastoid bone mass, S100 marker, CD1a marker. Birbeck granules

102
Q

Ticagrelor dangerous side effect

A

Neutropenia

103
Q

Cilostazol, dipyridamole

A

Phosphodiesterase III inhibitors that increase platelet cAMP, preventing ADP receptors from functioning. Also causes vasodiltation. DUAL EFFECT.

104
Q

Abciximab, eptifibatide, tirofiban

A

GpIIb/IIIa inhibitors

105
Q

B-lactamases location

A

Periplasm

106
Q

Mycolic acid is detected by what in an acid-fast stain?

A

Carbofuchsin

107
Q

Stains

A

Giemsa - Malaria + parasites (including intracellular) Ziehl-Neelson (carbol fuchsin) - Acid-fast bacteria, protozoa India Ink or Mucicarmine - Cryptococcus Silver Stain - Fungi, legionella, H. pylori

108
Q

Special culture requirements

A

Chocolate: h.flu Thayer-Martin: Neisseria (vanc, colistin, trimeth, nystatin) Regan-Lowe (+Bordet-Gengou): Bordetella Tellurie or Loffler - “Ill tell you right now, its diptheriae” Eaton agar - Mycoplasma pneumo (cholesterol) MacConkey-lactose fermenters Eosin-methylene blue - Ecoli Charcoal/cystein/iron - legionella Sabouraud: fungi

109
Q

AminOglycocydes (streptomycin, etc) ineffective against:

A

aerobes, requires O2 to enter cell

Only use for severe gram (-) rod infections

110
Q

Obligate aneorobes

A

Really chilly and cold: Ricketsia, chlamydia, coxiella

111
Q

Urease positive

A

PUNCH-K: Pseudomonas Ureaplasma Nocardia Cryptococcus H. pylori Klebsiella

112
Q

Catalase positive

A

Cats Need PLACESS: Nocardia Listeria Aspergillus Candida E.coli Staph Serratia

113
Q

Bacterial virulence factors

A

Staph aureus - Protein A SHiN - IgA protease GBS - M protein

114
Q

All exotoxins except one are destroyed at temps above 60C. What is that exotoxin?

A

Staphylococcal entertoxin. Also, endotoxin (gram negatives) is stable at 100C for 1hr

115
Q

Exotoxins

A
  • Diptheria and Pseudomonas inactivate EF-2 - Shigella and EHEC inactivate 60S ribosome by removing adenine from rRNA - ETEC has LT, ST; Vibrio cholerae has the equivalent of a LT toxin, except it PERMENTANTLY activates Gs (labile in the cAir, stabile on the cGround) - Bacillus anthracis and Bordetella have a toxin that mimics adenylate cyclase - Bordetella has a LT toxin equivalent, but does so by DISABLING Gi - Clostridium tetani and botulinum cleave SNARE - Clostridium perfringes (Alpha toxin) and Strep pyogens (ASO) degrade cell membrane - Staph aureus (TSST-1), Strep pyogenes (exotoxin A) bind MHC II/TCR –> IL1, IL2, IFN-y, TNFa –> shock
116
Q

Toxins encoded by lysogenic phage

A

Shiga-like toxin (EHEC) Botulinum toxin Cholera Diptheria Erythrogenic toxin of GBS

117
Q
A

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