Lessons Learned Flashcards

1
Q

Normal age-related cardiac changes

A

Decreased L ventricle chamber size
Sigmoid-shaped ventricular septum
Increased interstitial connective tissue
Lipofuscin pigment w/in macrophages

Decreased compliance of aorta & proximal major branches may lead to isolated systolic HTN

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2
Q

Compare the endogenous opioids

A

Mu- endorphins, morphine

Delta- enkephalins, DPDE

Kappa- dynorphins, ketazocine

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3
Q

Holiday Heart syndrome

A

Atrial fibrillation induced by binge drinking

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4
Q

Describe the 3 types of GABA receptors

A

GABAa- found in the brain; ion channel; causes Cl- influx when stimulated

GABAb- found in brain; G-Protein; causes K+ efflux, decreases Ca2+ influx, and inhibits adenylyl cyclase when stimulated

GABAc- found in retina; ion channel; causes Cl- influx when stimulated

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5
Q

Deficiency of which vitamin mimics Friedriech ataxia?

A

Vitamin E (posterior column & spinocerebellar tract demyelination)

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6
Q

Dysphagia + recent travel to South America

A

Think Chagas disease!

Trypanosoma cruzi, spread by Rediviid bugs

Tx: Nifurtimox

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7
Q

What conditions precipitate gallstones?

A

Elevated cholesterol/bilirubin
Decreased bile salts
Gallbladder stasis

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8
Q

Dysphagia + koilonychia

A

Iron deficiency anemia

Think Plummer-Vinson Syndrome + spoon nails

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9
Q

Mutation responsible for achondroplasia

A

Fibroblast Growth Factor Receptor 3 (FGFR 3)

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10
Q

Hepatocytes with ground-glass appearance

A

Hepatitis B

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11
Q

Stewart-Treves Syndrome

A

Cutaneous angiosarcoma in the context of chronic lymphedema

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12
Q

IgA nephropathy vs Acute Poststreptococcal glomerulonephritis

A

Both nephritic syndromes

IgA Nephropathy (Berger’s disease)- related to Henoch-Schonlein disease

  • Presents days after infection
  • Normal complement levels

Acute poststreptococcal glomerulonephritis

  • Develops weeks after infection
  • Low complement levels
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13
Q

Key players in Type IV hypersensitivity reactions

A

Macrophages, CD4+, CD8+, & natural killer cells

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14
Q

Compare homocysteinuria vs Marfans

A

Homocysteinuria- AR; downward lens dislocation; tight joints; mental retardation; heart uninvolved

Marfans- AD; upward lens dislocation; loose joints; normal intellect; aortic incompentence may occur

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15
Q

Supplement isoniazid treatment with:

A

Vit B6 (pyridoxine)

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16
Q

Orotic aciduria

A

Inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway) due to defect in EITHER orotic acid phosphoribosyltransferase OR orotidine 5’-phosphate decarboxylase

Autosomal recessive

Findings: increased orotic acid in urine, megaloblastic anemia (unimproved w/ B12 or folic acid), failure to thrive. NO HYPERAMMONEMIA (contrast w/ OTC deficiency)

Tx: Oral uridine administration (converts to UMP, which provides feedback inhibition to CPS II :. decreasing orotic acid production)

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17
Q

Ideal agent to treat hypertension plus osteoperosis

A

Hydrochlorothiazide (increases reabsorption of Ca in distal convoluted tubules)

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18
Q

Key mediator of septic shock

A

TNF-alpha

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19
Q

Councilman body

A

Eosinophilic globule indicative of hepatocyte apoptosis

Seen in acute viral hepatitis, yellow fever

20
Q

Hormone that causes hypercalcemia in squamous cell carcinoma

A

Parathyroid hormone related peptide (PTHrP)

Causes Humoral Hypercalcemia of Malignancy

21
Q

Effect of competitive vs noncompetitive inhibitors on Vmax & Km

A

Vmax- proportional to enzyme concentration
Km- affinity of enzyme for substrate

Competitive inhibitors increase Km; Vmax is unchanged; decreases potency

Noncompetitive inhibitors decrease Vmax but Km is unchanged; decreases efficacy

22
Q

Monosaccharides –> Disaccarides

A

Glucose + glucose = maltose

Glucose + fructose = sucrose

Glucose + galactose = lactose

23
Q

Treatment for pheochromocytoma

A

Phenoxybenzamine- non selective α-blocker

24
Q

Hypocalcemia + shortened 4/5th digits

A

Albright’s hereditary osteodystrophy

Pseudohypoparathyroidism

25
Q

Therapeutic use of interferons

A

Glycoproteins synthesized by virus-infected cells block replication of DNA & RNA viuses

Use: IFN-alpha: chronic hep B & C, Kaposi’s sarcoma
IFN-beta: MS
IFN-gamma: NADPH oxidase deficiency

Toxicity: neutropenia

26
Q

Hypnotic w/ lower risk of dependence

A

Nonbenzodiazepine hypnotics

Zolpidem, Zaleplon, Eszopiclone

Act via BZI receptor; reversed by flumazenil

Toxicity: ataxia, HA, confusion; short duration due to rapid metabolism by liver enzymes

27
Q

Kussmaul Sign

A

Paradoxical rise in JVP w/ inspiration

Indicative of constrictive pericarditis

28
Q

Elevated 14-3-3 protein in CSF

A

Creutzfeldt-Jakob disease

29
Q

Branched chain amino acids

A

Isoleucine
Leucine
Valine

30
Q

Unique components of smooth muscle contraction

A

Calmodulin (bound by Ca to activate MLCK)

Myosin light-chain kinase –> Myosin P + actin –> CONTRACTION
*Nitric oxide increases cGMP :. inhibits MLCK

Myosin light-chain phosphatase –> Myosin + actin –> RELAXATION

31
Q

Hepcidin

A

Central regulator of iron hemostasis (binds ferroportin to prevent intestinal absorption of iron & to prevent macrophage release of ferritin)

Acute phase reactant synthesized by hepatocytes

32
Q

Malignant hyperthermia

A

AD sensitivity to inhaled anesthetics

Defective ryanodine receptor on sarcoplasmic reticulum releases excessive Ca into mm cytoplasm –> elevated ATP reuptake in SR

Tx: Dantrolene

33
Q

Fanconi syndrome vs Fanconi anemia

A

Fanconi anemia: genetic defect in DNA repair –> AML, bone marrow failure; congenital defects (short stature, abnormalities of skin/arms/head/eyes/kidneys/ears), developmental disabilities

Fanconi syndrome: disease of proximal tubules where glucose, amino acids, uric acid, phosphate, & bicarb pass into urine instead of being reabsorbed; causes proximal renal tubular acidosis

34
Q

Profound hypochlorhydria + increased serum gastrin

A

Pernicious- anemia induced atrophic gastritis

35
Q

Methods to reduce risk of tumor lysis syndrome

A

Aggressive hydration

Rasburicase (recominant urate oxidase; converts uric acid to allantoin for excretion)

Allopurinol

TLS: oncologic emergency during chemo where rapid cell turnover leads to massive release of intracellular ions (potassium, phosphorous)

36
Q

Weil’s Disease

A

Infection w/ leptospira interrogans –> jaundice, azotemia, fever, hemorrhage, & anemia

37
Q

ITP vs TTP

A

Both decrease platelet count, decrease platelet survival, & increase bleeding time

ITP- Defect in anti-GpIIb/IIIa antibodies –> peripheral platelet destruction
Labs show increased megakaryocytes

TTP- Deficiency of ADAMTS 13 (vWF metalloprotease) –> decreased degradation of vWF multimers
Labs: schistocytes, elevated LDH
Pentad of symptoms: neurological symptoms, renal symptoms, fever, thrombocytopenia, & microangiopathic hemolytic anemia

38
Q

Name the hepatitis viruses

A

HAV- RNA picornavirus

HBV- DNA Hepadnavirus

HCV- RNA flavivirus

HDV- RNA delta virus

HEV- RNA hepevirus

39
Q

Serotonergic neurons are found in. . .

A

the RAPHE NUCLEUS in the brainstem

40
Q

Which parts of the kidney are most susceptible to hypoxia?

A

Proximal tubules & thick ascending limb of loop of Henle (both located in outer medulla)

41
Q

Renal pathology associated w/ sickle cell disease

A

Papillary necrosis

42
Q

Reactions involving biotin

A

Biotin = B7
Used as a cofactor for carboxylation enzymes (add 1-C group)

1- Pyruvate carboxylase: Pyruvate (3C) –> oxaloacetate (4C)

2- Acetyl CoA carboxylase: Acetyl CoA (2C) –> malonyl CoA (3C)

3- Proprionyl CoA carboxylase: Propionyl-CoA (3C) –> methylmalonyl-CoA (4C)

43
Q

B6 is needed to synthesize:

A

cystathionine, heme, niacin, & GABA

(B6 is converted to pyridoxal phosphate, which is also used in transamination, decarboxylation, & glycogen phosphorylase)

44
Q

Atypical cells seen during EBV infection

A

Reactive cytotoxic T cells

*They hug the RBCs!

45
Q

Which part of the lymph node isn’t well developed in DiGeorge Syndrome?

A

Paracortex

46
Q

Defect in xeroderma pigmentosum

A

UV-specific endonuclease