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USMLE > UWorld Renal and Heme > Flashcards

UWorld Renal and Heme Flashcards

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USMLE® Step 1 flashcards
1
Q

Define Heteroplasmy

A

Presence of different organellar genmoes within a single cell (mutated and wild). Severity of mitochondrial disease often related to proportion of abnormal to normal mitochondria within pt. cells

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2
Q

Pleiotropy

A

Single gene can lead to multiple phenotypic manifestations

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3
Q

Linkage Disequilibrium

A

When a pair of genes are inherited MORE OR LESS often than by random chance - this can occur EVEN if genes are on different chromosomes

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4
Q

Periodic nonperistaltic contractions of esophagus (name and s/sx?) vs GERD

A

Diffuse esophageal spasm (DES) - in DES severeal segments of esophagus contract at same time (as oppose to just above bolus), preventing propoagation of bolus. These can be painful. S/Sx - intermittent dysphagia and occasional chest pain. Complete cardiac workout required to rule out cardiac cause. Different from GERD in that GERD is BURNING, DES is CRAMPY.

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5
Q

Medical mistake - what to do?

A

Tell pt immediately

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6
Q

Candida - yeast, mold, or both? Presentation in HIV patients? When do you see disseminated candidiasis?

A

Yeast w/ pseudohyphae.Easily disrupted chains of cells. IN HIV, T cells lacking - usu superficial infections (trush, cutaneous, vulvovaginits). N! prevent hematogenous spread. See disseminated candidiasis in neutropenic pt (and those w/ inherited impairments of phagocytosis. HIV+ w/ neutropenia have risk for localized and disseminated candidiasis. Disseminated ex (right sideded endocarditis, liver/kidney abscesses, candidemia). Summary: Local defense (Tcells), Systemic defense (N!)

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7
Q

What complement problems dispose pt to infections and SLE-like disease? What predispose individuals to Neisseria gonorrhea/meningitidis?

A

C1,2,4 to infections/SLE-like. C5,6,7,8,9 to both Neisseria

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8
Q

Hypogammaglobulinemia predisoses to?

A

Bacterial infections. And thus not cadida or anything else.

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9
Q

Lac operon regulated by?

A

Negatively by binding of represor protein to operator locus; Positively by cAMP-CAP binding upstream from promoter region. If you have mutations that impair binding of Lac I (repressor protein - think “inhibitor”) to its regulatory sequence in operator region you have lac consitutively expressed.

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10
Q

Constipation common which 3 groups? How do you treat these 3 groups?

A

Elderly, debiliated, chronic opioid therapy. Usu life-modification not an options, to streat w/ osmotic laxatives - ethylene glycol, magnesium hydroxide (questionable)

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11
Q

Describe Diarrhea in IBD, Crohns, Diarrhea, Rectal prolapse. Lactase deficiency

A

Crohns - Diarrhea of secretory type - characterized by high electrolyte content due to poor absorption and INC loss from inflamed intestinal mucosa. IBD - diarrhea alternating w/ constipation, ab pain, distention, fecal and water electrolyte content is NORMAL. Pooping helps pain. Carcinoid syndrome - secretory and high in electrolytes. Rectal prolapse- assoc w/ pregnancy/constipation - can be seen in SEVERE diarrhea - Cystic fibrosis (esp childrne). Lactase def (lactose not broken down to glucose/galactose) -> osmotic

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12
Q

Bloating, fullness, indigesetion. + guaiac test.

A

Likely peptic ulcer disease. Most common location - proxmial duodenum, antral stomach, GE junction. Malignant duodenal ulcers RARE. Gastric ulcers can FREQUENTLY be malignat.

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13
Q

Matching - used where and for what purpose?

A

Matching - using in case control - helps limit confounding.

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14
Q

DEC MHC1. Found when. Reprecussions?

A

Found in viral infected and tumor cells - Leads to NK cell destruction- INDUCED APOPTOSIS. NK do not express CD4,8, 3. Express CD16 or 56. Do NOT require thymus for maturation (prsent in athymic pt - derived from lymphoid stem cells), no antigen-specific activities. Activated by INFgamma andIL12.

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15
Q

Majority of gastric ulcer occur where? Why? Complications

A

Lesser curvature of stromach - border between acid secreting (corpus) and gastrin secreting (antrum) mucus. Left and right gastric arteries likely to be penetrated.

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16
Q

Diphenoxylate? Mechanisms, Tx for? What is Tx for secretory diarrhea?

A

Diphenoxylate - opiate -anti-diarrheal structurally relatd to meperidine. Binds to mu opiate recptors in GI tract and slows motility. Low doses allow for antidiarrheal effects w/o sig opiate effects. Low doses packaged w/ atropine(Lomotil) - sided effects (bloating mild sedation) Secretory diarrhea can be treated w/ octreotide?!

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17
Q

What do you need to supplemet total gastrectomy pt with. Why?

A

Not gastric enzymes or HCL - can proceed normally in absence of pepsin - not triglycerides (can passively diffuse through GI lumen, although best absorbed as monoglycerides. Not fat soluble vitamins. NEED TO GIVE WATER SOLUBLE VITAMINS (B12) due to lack of intrinsic factor (parenteral)

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18
Q

Describe midgut fetal development

A

Midgut herniates through umbilical ring at 6 week to allow for rapid growth of intestines/liver despite slower growth of ab cavity. Midgut returns 10th week of fetal life, takes 270 degree counterclockwise rotation around SMA. If MALROTATION occurs - cecum found in right upper quadrant fixed by fibrous bands (Ladd’s bands) - these bands often compress duodenum - bilious vomiting in early days. Twisting around SMA can also lead to midgut volvulus w/ intestinal gangrene

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19
Q

Omphalomestenteric duct role

A

Connects lumen of midgut w/ yolk sac - failure to obliterate causes vittelline fistula. Partial failure causes Meckel diverticulum

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20
Q

Describe hindgut fetal development

A

Hindgut descents after midgut returns to ab cavity. As intestines growh, ascending and descending are pressed agasint posterior wall and are fized in position.

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21
Q

Brunner glands?

A

Unique to duodenum - secrete alkaline solution into crypts of Lieberkuhn - deep to submucosa and muscular mucosa

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22
Q

Peyers patches

A

lymphoid aggregates specific to ILEUm

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23
Q

Can patients withhold information about their care/biopsy result to themselves and family?

A

Yes. Must make sure they are not depressed or incapacitated tho.

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24
Q

Bleed, PTT and PT times

A

2-7 minutes, 25-40 seconds, 11-15 seconds

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25
Q

Hemarthrosis and prolonged bleeding (tooth extraction etc) suggestive of?

A

Clotting factor defect

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26
Q

vWF deficiency inheritance - clinical findings - lab findings.

A

AR - F8 and platelet binding problem - INC PTT and Bleeding time.

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27
Q

Hagemen factor deficiency clinical presentation?

A

F12 def. INC PTT, usu does NOT cause clinical bleeding though

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28
Q

Hemophilia A vs B? Inheritance?

A

A = 8. B = 9. Both are X linked recessive. Why you see more in males.

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29
Q

Transient numbness and tingling in body part that resovles in 20 minutes. Treatment

A

TIA. Tx w/ low dose aspirin.

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30
Q

COX activity in platelets and endothelial cells. What does COX work on?

A

Platelet - COX works on PGH2 to produce TXA2 - platelet agg. Endothelial cells - COX works on PGH2 to produce PGI2 -> inhibits agg.

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31
Q

Samter Triad?

A

Aspirin hypersensitivity - causes flushing, nasal polyps and symptoms, and bronchospasm in patients w/ 10% of ASHMATICS treated w/ aspirin

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32
Q

Very High Dose spirin

A

Vertigo, Tinnitus, Hearing Loss (salicylism) - can also stimulate respiratory drive (hyperpnea), leading to metabolic acidosis GI bleeds!

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33
Q

Low dose aspirin

A

GI bleed, INC uric acid levels (at high doses, Uric acid is DECREASED.

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34
Q

Tx for LONG TERM DVT OR PE maintenance

A

Warfarin - not heparin. inhibits vitK dependent gamma carboxylation. Heparin is drug of choice for ACUTE management (activates AT3)

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35
Q

Direct thrombin inhibitors. How do they work. What do they do. How is this different from heparin?. Examples of DTI

A

DTI binds to thrombin active site and thus do not require AT3 as heparin does, be anticoag. Directly inhibit thrombin mediated fibrin formation. Examples - Argatroban, hirudin, lepirudin

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36
Q

Ab pain, arthralgias, proteinuria, positive occult stool, palpable trunk lesions. Age range? How does this differ from meningococemia?

A

HSP - IgA - immune complex deposition. Affects kids between 3 and 10. Meningiococemia has skin rash on trunk and legs as well, but also has fever hypotension, tachy etc.

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37
Q

Delayed hypersensitivity. What to think?

A

Granulomas - macrophage dependent - fungi and TB.

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38
Q

Parvovirus b19

A

noneveloped - ss DNA

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39
Q

GN sepsis pathology. Schistocytes or no schistocytes?

A

activation of coag cascade by endotoxin - causes widespread fibrin deposition and consumption of factors, platelets, and bleeding. microemboli, schisotcytes

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40
Q

When are target cells seen?

A

obstructive liver disease, thalassemia, iron deficiency, asplenism

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41
Q

Acanthocytes (Burr cells) vs Teardrops

A

abetalipoproteinema/valve trauma, extreme form is spur cells. Teardrops seen in myelofibrosis

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42
Q

Cell interactions during Rolling, Crawling/Tight Adhesion, and Transmigration

A

Rolling - N! (Sialyl Lewis, L selectin), endothelial (E/P selectin). Crawling/Tight Adhesion - N! (CD18B2 integrin Mac-1, LFA-1), endothelial cells (ICAM). Transmigration (platelet endothelial cell adhesion molecules - PECAM1, found on intercellular junctions of endothelial cells (crawling inwards)

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43
Q

Delayed umbilical separation, bleeding complications. No pus formation

A

leukocyte adhesion deficiency (LAD) - leuks lack CD18 (inability to synthesize B2 integrins Mac 1 and LFA1.

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44
Q

Where are T cells and dendritic cells located in LN? When do you see a def in this region?

A

paracortex. See def w/ DiGeorge syndrome

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45
Q

Medullar sinuses and cords of LN contain?

A

B cells plasma cells, M!

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46
Q

When would you see no cortex/germinal centers?

A

In agammaglobulinemia - no B cells, no GC, no primary follicles

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47
Q

B12 nutritional def - shows up when? Where is it stored? Folate? Vitamkin K?

A

After absent for multiple years due to large hepatic stores. Liver stores about 1/2 of bodies folate. Folate runs low after 3-4 months. Liver has 1-3 weeks store - but this is usu not a prob due to intestinal bacterial production

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48
Q

vWD inheritance? Hemophilia inheritance? Lab change for both?

A

vWF- AD. Hemophilia - X linked R. Both have elevated PTT times. However, Hemophilia does NOT have prolonged bleeding time, whereas vWD has prolonged bleeding time

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49
Q

Clopidogren, Ticlopidine mech

A

Irreversibly bind ADP receptor

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50
Q

Dipyridamole, cilostazol

A

inhibit platelet aggregation by inhibitindg PDE activity and INC cAMP

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51
Q

abcixamab, eptifibatide, tirofiban mech

A

Gp2b/3a inhibitors

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52
Q

How to treat HIT?

A

Heaprin is number one cause of thrombocytopenia in hospitals -t reat with direct thrombin inhibitors.

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53
Q

Hydroxyurea and SS? Mech? Also prevent intracellular dehydration (leading to sickling, with what?)

A

INC Hemoglobin F synthesis. Prevent intracellular dehydration w/ Gardos blockers (calcium dependent potassium channel blockers)

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54
Q

Haldane and Bohr Effect

A

Haldane - As O2 INC, CO2 and H are unloaded. Bohr - As H and CO2 INC, O2 unloads

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55
Q

What causes hematomas to turn green after a few days?

A

Heme oxygenase - converts heme to to biliverdin (greenish).

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56
Q

master control of iron levels

A

Hepcidin (liver cells)! Controls enterocytes by controlling ferroprotin downregulation etc

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57
Q

When does sickling happen in SS?

A

Sickling precipitated by low oxygen levels, INC acidity, low blood volumes. So greater chance of also where blood moves slowly in organs - spleen, liver, kidney. More likely to aggregate upon oxygen unloading. OXYGENATED HB DOES NOT SICKLE

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58
Q

G6PD inheritance? Inability to form what later down the line?

A

X linked recessive- disorder of hexose monophosphate pathway - results in hemolytic anemia due to oxidative stress. UNABLE TO PRODUCE 6-PHOSPHOGLUCONATE

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59
Q

COX2 inhibitors - effects?

A

anti-inflam w/o ulcers/bleeding. ALSO VERY LITTLE BLOCKAGE OF PLATELET AGG, as platelets mainly express COX1.

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60
Q

persistent fever, bleeding gums, sore throat

A

AML (neutropenia so can get fever and infections, bleeding gums from thrombocytopenia) See myeloblasts - abundant basophilic cytoplasm - nuclei folded or biloped, may contain multiple nuclei - Auer rods stain for myeloperoxidase.

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61
Q

How to differentiate CML from leukemoid reaction?

A

Both have INC WBC cell, but CML is alkalkine phosphatase negative. Definitive diagnosis of CML requires 9:22 (phl) chromosome. CML also often have basophilia.

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62
Q

14;18 translocation what problem and what do each gene stand for?

A

Follicluar Lymphoma - Bcl2 and heavy chain

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63
Q

Bcr-abl. What problem

A

CML philly 9:22.

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64
Q

In heme disorders, if you have to guess inheritance, think structural is what and enzyme def is what?

A

Structural (adutosomal dominant - e.g. hereditary spherocytosis)Enzyme - (autosomal recessive). Although G6PD is x linked recessive

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65
Q

Vitamin D resistant rickets inheritance pattern

A

X linked DOMINANT. (fairly unusual)

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66
Q

Blast appear? What stain?

A

Blue and large. Blue from ribosomal RNA after Wright Giemsa stain.

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67
Q

Cause of death in children w/ bilateral renal agenesis. How long do they live for?

A

If carried to term and delivery, death is due to lung immaturity. Die within a hours of birth

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68
Q

VHL mutation - can lead to? Genetic factor?

A

Renal Cell Carcinoma - VHL mutation can be inherited or acquired. DELETIONS on chr3!!!

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69
Q

What chromosomes are RB, NF1, WT-1 (Wilm’s tumor). What does BRCA1 do? VHL mutation?

A

13, 17, 11. BRCA1 INC risk of breast and ovarian CA. VHL 3.

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70
Q

What internal part is directly next to 12th rib?

A

Left kidney

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71
Q

What ribs overly the spleen?

A

9,10,11

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72
Q

ADH stimulates what specific receptor? What affect? Where does this occur?

A

EIther V1 or V2. V1 vasoconstricts and is prostaglanding secreting. V2 has antidiuretic effects. Occurs at the medullary segment of collecting duct

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73
Q

Where is the interstitial osmolality the highest?

A

Medullary interstitium

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74
Q

Interplay between ADH (high) and urea?

A

ADH upregulates passive urea transporters in the inner medulary collecting duct. Further INC osmolality of interstitium

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75
Q

Where is lithiums effect on the kidney? When would you see this?

A

Pt w/ bipolar. Lithium leads to Diabetes Insipidus - ADH does not work on the medullary collecting duct.

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76
Q

Disease of T2 RPGN

A

All things that have immune COMPLEXES - PSGN, SLE, IgA neprhopathy, Henoch Schonlein Purpura

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77
Q

Disease of T 3 RPGN

A

Wegners (granulomatosis w/ polyangiitis)

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78
Q

When do you see DEC C3 levels?

A

During alternative pathway activation - seen in PSGN and other T2 RPGN disease w/ complement deposition

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79
Q

When do you see DEC in C4 levels

A

C1 esterase inhibitors deficiency, which triggers the classical pathway, and leads to DEC C4 levels by breakdown from c1 esterase. Seen in hereditary angioedema

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80
Q

Def of Filtration Fraction?

A

GFR/renalPLASMA flow.

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81
Q

CLEARANCE formula?

A

Urine conc*Urine volume all divided by plasma conc

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82
Q

PAH approximates?

A

renal plasma flow

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83
Q

GFR approximated by?

A

inulin or creatinine

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84
Q

Formula related renal plasma flow to renal blood flow (taking into account hematocrit?)

A

(1-hematocrit)(RBF)=RPF

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85
Q

Angiomyolipomas associated with?

A

Tuberlous sclerosis. Bilateral angiomyolipomas is TS 90% of the time. TS is AD,

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86
Q

Clinical findings of NF1 and inheritance pattern?

A

AD - neurofibromas, optic gliomas, pigmented iris (Lisch nodules), hyperpigmentation spots (cafe-au-lait)

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87
Q

Clinical findings of NF2 and inheritance pattern

A

AD - bilateral acoustic neuromas, multiple meningiomas, gliomas, and ependymomas of spinal cord

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88
Q

Von Hippel Lindau clinical findings and inheritance pattern

A

AD - cerebellar hemangioblastomas, retinal hemangiomas, liver cysts, plus high risk for bilateral RCC.

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89
Q

Capillary angiomas of face and choroid. Think? Other assoc? Inheritance pattern?

A

STurge Weber. Also leptomeningial angioma, glaucoma, MR, seizures. Sporadic (likely somatic) mutation.

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90
Q

Multiple telangiectasias on skin and mucosa. Think? Clinical Findings? Inheritance?

A

AD - Hereditary Hemorrhagic telangiectasias (Osler Rendu Weber) - recurrent epistaxis or GI bleeds

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91
Q

Inheritance of NF1, NF2, Tuberlous Sclerosis, Sturge Weber, VHL, Hereditary Hemorrhagic Telangiectasia?

A

All are AD except Sturge Weber, whcih is sporadic

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92
Q

Pts (5)with INC risk of acute leukemia?

A

Downs, Fanconi, Patau, Ataxia-telangiectasia, Bloom syndrome

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93
Q

Skin lesions with fibroblasts that fail to metabolize ceramide trihexoside.

A

Fabry disease - (angiokeratoma corporis diffusum) - Inherited deficiency of alpha -galactosidease A. Globoside ceramide trihexoside accumulates in tissues. S/Sx - Hypohidrosis, acroparesthesia, angiokeratomas. Acroparestheisa is episodic burning neuropathic pain in extremities. Angiokeratomas are punctuated dark red NONBLANCHING macules and papules that occur between umbilicus and knee. Without enzyme replacement tehrapy, progressive renal insufficiency -> failure.

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94
Q

When is mannitol used? What can be a problem with mannitol? Who are high risk?

A

Usu not used as a diuretic. Instead, used as osmotic diuretic in pt w/ cerebral edema or INC ICP. Excessive tx w/ osmotic diuretics can lead to excessive volume depletion and eventual hypernatremia in pt. Problem w/ mannitol is that it can cause PULMONARY EDEMA - this is from rapid rise in volume that INC HYDROSTATIC pressure pressure. Be careful of use in pts with CHF or preexisting pulmonary edema.

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95
Q

Thiazide duretic tox

A

Hypokalemia and hypomagnesemia (think GIttelman syndrome) Less commonly causes hypercalcemia

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96
Q

Bumetanide? What is it?

A

Loop diuretic that inhibits NKCC. Loop diuretics also can cause hypokalemia, hypomagenisemia (like thiazide), BUT these cause hypocalcemia, not hypercalcemia.

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97
Q

Side effets of spironolactone

A

aldosterone antagonist - significant hyperkalemia, gynecomastia, DEC libido, ED.

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98
Q

Triamterene?

A

Potassium sparing diuretics - blocks ENAC in DCT and collecting duct.

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99
Q

Angiomyolipomas associated with?

A

Tuberlous sclerosis. Bilateral angiomyolipomas is TS 90% of the time. TS is AD,

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100
Q

Acyclovir toxicity? Presentation?

A

Nephrotoxicity! Pricinpally excreted in urine via filtration and secretion. When acyclovir [conc] in collecting duct exceeds solubility, you get damage via CRYSTALLINE NEPHROPATHY . This can be treated w/ adequate HYDRATION and dose adjustment. May present as delirium/tremor.

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101
Q

Amphotericin toxicity? Lab findings of tox?

A

Renal toxicity - causes renal vasoconstriction and DEC GFR. Also may act as direct toxin and cause ATN. severe HYPOKALEMIA AND HYPOMAGENSEMIA CAN BE SEEN. This is a reflection of INC in distal tubular membrane permeability. Requires daily supplementation

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102
Q

Calcineurin? Function?

A

Essential protein for activation of IL-2 which promotes growth and diff of T cells. Immunosuppressants such as CYCLOSPORIN and Tacrolimus work by inhibiting calcineurin activation. (Calcineurin dephosphorylates NFAT, which binds to IL2 promotor. THis is why you give calcinerin inhibitor sto those w/ T cell mediated acute transplant rejection

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103
Q

Capillary angiomas of face and choroid. Think? Other assoc? Inheritance pattern?

A

STurge Weber. Also leptomeningial angioma, glaucoma, MR, seizures. Sporadic (likely somatic) mutation.

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104
Q

Vasopressin. Relation to Urea?

A

Vasopressin stimulates V2 receptor, which INC permeability of water and urea in medullary colelcting duct - This INC in urea reabs leads to DEC renal clearance of urea and DEC fractional excretion.

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105
Q

Inheritance of NF1, NF2, Tuberlous Sclerosis, Sturge Weber, VHL, Hereditary Hemorrhagic Telangiectasia?

A

All are AD except Sturge Weber, whcih is sporadic

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106
Q

Pts (5)with INC risk of acute leukemia?

A

Downs, Fanconi, Patau, Ataxia-telangiectasia, Bloom syndrome

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107
Q

Acetazolamide toxicity?

A

somnolence, paresthesia,s urine alkalization

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108
Q

Bumetanide? What is it?

A

Loop diuretic that inhibits NKCC. Loop diuretics also can cause hypokalemia, hypomagenisemia (like thiazide), BUT these cause hypocalcemia, not hypercalcemia.

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109
Q

Side effets of spironolactone

A

aldosterone antagonist - significant hyperkalemia, gynecomastia, DEC libido, ED.

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110
Q

PSGN - how does it look on light microscopy. Whats lab findings?

A

hypercellular - due to leukocyte infiltration and mesangial and endothelial cell proliferation. EM shows humps and bumps. IgG and C3 deposits. Leading to Low c3 levels, low total complement levels, elevated anti-DNAse B titers, resence of CRYOGLOBULINS. C4 usually normal.

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111
Q

Hypoxia induced lactic acidosis - what enzyme activity changes are associated with this?

A

Low pyruvate dehydrogenase and high lactate dehydrogenase activity.Side note, Pyruvate carboxylase leads to oxaloacetate.

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112
Q

Effect of Uremia on endocrine?

A

Can lead to DEC peripehral tissue conversion of T4 to T3 -> can produce functionally hypothyroid state

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113
Q

Gross painless hematuria in older adult. What until proven otherwise? What do the cells look like?

A

Urothelial Ca w/ ronded/polygonal cells w/ abundant clear cytoplasm. As they are clear from staining, this usually suggest high conc of dissolved LIPIDS AND GLYOCGEN

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114
Q

Digoxin. Cleared by?

A

Kidneys. Which is why you have to be careful of digoxin toxicity in elderly, who naturally have age-related renal insufficiency.

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115
Q

If you constrict efferent arteriole, what is the result on GFR, FF? Why? Think this through

A

INC GFR, INC FF.

116
Q

When do you worry about ototoxicity in the context of renal stuff?

A

Ototoxic agents (aminoglycosides, salicylates, cisplatin), loop diuretics -furosemide) - Especially if these are stacked. Aminoglycosides are oto and neprhotoxic too.

117
Q

What diuretics are used in an acute setting? Such as acute decompensated CHF?

A

Loop diuretics - give max amount of diuresis in shortest period of time.

118
Q

Acetazolamide toxicity?

A

somnolence, paresthesia,s urine alkalization

119
Q

Rule of thumb relationship between GFR and creatinine?

A

Every time GFR halves, serum creatinine doubles

120
Q

Where is PAH concentration the lowest in nephron? Why?

A

PAH conc is lowest in bowmans space. It is not reabs, just secreted. so lowest at the beginning

121
Q

What drugs are assoc w/ cardiac muscle cell damage?

A

doxorubicin, daunorubicin.

122
Q

Drugs that can lead to liver necrosis?

A

Acetaminophen, halothane

123
Q

Working in rubber factory is a risk for?

A

Transitional cell CA of bladder

124
Q

In rapidly progressive glomerulonephritis, what are the crescent formations made of?

A

Glomerular parietal cells, monocytes, macrphages, abundant fibrin.

125
Q

Hypoxia induced lactic acidosis - what enzyme activity changes are associated with this?

A

Low pyruvate dehydrogenase and high lactate dehydrogenase activity

126
Q

Effect of Uremia on endocrine?

A

Can lead to DEC peripehral tissue conversion of T4 to T3 -> can produce functionally hypothyroid state

127
Q

Gross painless hematuria in older adult. What until proven otherwise? What do the cells look like?

A

Urothelial Ca w/ ronded/polygonal cells w/ abundant clear cytoplasm. As they are clear from staining, this usually suggest high conc of dissolved LIPIDS AND GLYOCGEN

128
Q

Embryology, what gives rise to parts of the neprhon?

A

Ureteric bud - collecting tubules, ducts, major and minor calyces, renal pelvis, ureters>Metanephric mesoderm (blastema), - glomeruli, Bowman space, proximal tubules, loop of Henle, Distal Convoluted tubules

129
Q

When you see fatigability, constipation, bone pain renal failure in eldery pt think what?

A

MM. Fatigability (anemia), Constipation (hyperCa), bone pain (osteoclast activity and bone lysis), renal fialure . this can result in EOSINOPHIILIC CASTS - (myeloma kidney)due to excessive free light chains.

130
Q

What does chronic lead tox lead to in kidney?

A

chronic tubulointerstitial nephritis

131
Q

What diuretics are used in an acute setting? Such as acute decompensated CHF?

A

Loop diuretics - give max amount of diuresis in shortest period of time.

132
Q

Acute Tubular Necrosis? Etiology. Phasese

A

Ischemic or Nephrotoxic. Initiation, Oliguric phase (DEC GFR), Recovery (tubular re-epithelialization). Most patients regain function. If multi-organ failure occurs, interstitial scarring my be seen on light microscopy. Ischemic often written in as trauma or severe hypotension.

133
Q

Post-streptococcal GN. Patient population and outcomes?

A

Classic picture is kid 6-10y.o. 95% totally recover. Only 60% of adults totally recover.

134
Q

Immediate transplant failure called? Dude to?

A

Hyperacute rejection - antibody mediated. Among others, can be anti-ABO or anti-HLA ab. This is T2 HSR.

135
Q

Describe Immediate Hypersensitivity

A

This is T1 HSR - antigen leads to IgE class switching of B cells. Asthma, allergies, urticaria (hives). NOT immediate transplant rejection

136
Q

IF of PSGN shows what little particles causing lumps and bumps?

A

IgG, IgM, C3 in mesangium and basement membrane - produces “starry sky appearance”

137
Q

Working in rubber factory is a risk for?

A

Transitional cell CA of bladder

138
Q

Where in the nephron is tonicity the lowest in setting of HIGH ADH

A

DCT. It is impermeable to water but keeps pumping out salt. Pinnacle of the thick ascending loop.

139
Q

Minimal changes disease - why it this caused?

A

Specific cytokine damage causing effacement. This is why cortisol works.

140
Q

Selective proteinuria

A

albumin loss within macroglobulin or IgG loss.

141
Q

Tubular proteinuria

A

Damage to PCT. Usually reabs low molecular weight proteins (b2 microglobulin, Ig light chain, AA, retinol binding protein). If PCT is damaged you get these proteinsi n urine.

142
Q

Functional proteinuria

A

proteinuria due to changes in blood flow. Can be seen in young adults w/ normal renal failure after exercising, fever, cold exposure, emotional stress. Disappears upon retesting

143
Q

Orthostatic proteinuria

A

Happens in taller thin adolescents - INC protein excretion when standing, but normal when supine (Sleeping)

144
Q

Isolate dproteinuria

A

Incidental finding of asymptomatic pt w/ normal renal function and sediment.

145
Q

What is one standard deviation, 2 standard deviations

A

1 - 68. 2 - 95. 3 -99.7

146
Q

Chest pain, ab pain, bone pain

A

Sickle cell occlusions

147
Q

Most common cause of CF?

A

Genetic mutation - phenylalanine DELETION

148
Q

What is warfarin-induced skin necrosis caused by?

A

Protein C or S deficiency. Warfarin initially rapidly reduced Protein C/S and F7. If you have a def in C or S, this exaggurates the coagulation factors, and causes microthrombi that occlude vessels -> skin necrosis

149
Q

How to treat warfarin induced skin necrosis

A

Remove Warfarin, administer FFP to replenish protein C

150
Q

AT3 def inheritance? Effect

A

AD. Causes hypercoagulable state. HEP doesnt work as well.

151
Q

Raltegravir effect? For?

A

For HIV, impairs ability of HIV to integrate into host genome (integrase inhibitor) messanger RNA transcription

152
Q

What virus can cause cells (which) to transformation and immortalization

A

EBV infected B cells can cause B cell prolif. Can still secerete Ab.

153
Q

What are cryoglobulins and what do they contain?

A

cold precipitated serum proteins that contain Immunoglobulins. Most commonly assoc w/ HepC

154
Q

Hemadsoprtion. What is it and what is assoc w/ it

A

hemagluttinins or glycoproteins that have high affinity for RBC - are expressed on host surface. Assoc w/ influenza and parainfluenza

155
Q

How does Parvo virus attach/enter cells. What cells does it enter?

A

Via P antigen - found on basically all erythro-type cells, placenta, fetal liver and heart.

156
Q

How does EBV bind to B cells CD21

A

Via envelop glycoprotein gp350, binds to CD3d (CR2, CD21). Remember, EBV is still a herpes virus

157
Q

How do herpes virus enter cells? Including CMV

A

glycosaminoglycan chains onto host surface cell proteoglycans

158
Q

Explain HIV binding to Cells

A

HIV binds to CD4 cell. However, it requires CCR5 for entry. so those who are homozygous CCR5 absent, HIV can bind but not enter.

159
Q

What are Tat and Nef, HIV proteins?

A

Tat - plas a role in viral replication. Nef - DEC MHC1 on infected cells

160
Q

What is fibronectin. Where is it synthesized?

A

high molecular weight glycoprotein that binds to extracellular matrix and integrin protines. Synthesized in liver. Plays a role in wound healing

161
Q

Where does isotype switching occur?

A

In the germinal centers (in LN). After IgM initial response, B cells can change to something else.

162
Q

Where does VDJ recombination occur?

A

This happens in the bone marrow. You will not see VDJ happening in LN. Somatic hypermutation DOES happen in the LN though.

163
Q

Where does somatic hypermutation occur?

A

In the LN. Only VDJ is in bone marrow basically. Isotype switching is also in LN.

164
Q

What is the most commonly used heparin in hospital setting? How do you treat overdose of heparin?

A

Unfractionated heparin is used most in hospital. Treat overdose w/ PROTAMINE (sulfate), which binds HEP and forms a complex with no anticoag activity. Keep in mind that Protamine does NOT work w/ low molecular weight heparin.

165
Q

What is FFP used to reverse?

A

Warfarin overdose.

166
Q

What is aminocaproic acid used to reverse?

A

Inhibits plasminogen activation. Inhibit fibrinolysis. Both aminocaproic acid and tranexamic acid do this .

167
Q

Metronidazole side effects?

A

GI (nausea, vomiting, crampy ab pain) + neurologic (paresthesias, dizziness). Disulfiram rx w/ alcohol

168
Q

Vancomycin side effects/tox?

A

Dose dependent ototoxicity, also red-man syndrome

169
Q

Imagine Antibody. Where does complement, antigen, and APC/Fc bind?

A

Antigen binds to the Fab light chain. APC/Fb binds at the tail. Complement binds midway through of tail

170
Q

What is normal Ca serum levels

A

8.4 to 10.2 mg/dL

171
Q

Tingling toes and feet should make you think what metabolite def?

A

hypocalcemia

172
Q

Why is there citrate in packed blood. What is the problem with this?

A

Citrate acts as anticoagulant in packed blood. However, after multiple 5/6 transfusions, citrate can chelate Ca, leading to hypocalcemia

173
Q

What does pyruvate kinase def lead to?

A

Inability to generate ATp via glycolysis in RB leads to cells failing to maintain erythrocyte structure. PK Def leads to hemolysis. Can lead to splenic hypertrophy as it clears it from system.

174
Q

What do you see in Niemann Pick’s disease?

A

accumulation of sphingoyelin

175
Q

What do you see in Gaucher disease

A

accumulation of glucocerebrosides

176
Q

What is dapsone used in?SIde effects of dapsone

A

Antimalerial plus PCP if pt cant toelrate TMP-SMX. Side effects fever, rash, methemoglobinemia.

177
Q

Infliximab used to treat?

A

RA, ankylosing spondylosis, firstulizing Crohns disease. Works as antibody to TNF-a. DIfferent than rituximab (anti-Cd20)

178
Q

Ganciclovir - compared to acyclovir? Side effects?

A

Gangciclovir (CMV), reacts more w/ human cells than acyclovir. Side effects include neutropenia, anemia, thrombocytopenia (pancytopenia), and renal impairement. This all occurs ESPECIALLY when co-adminstered w/ ZIdovudine, which has the same mech as Gangciclovir - problems with DNA synthesis in hematopoietic stem cell lines

179
Q

Zidovudine

A

antiviral used in HIV. Side effect of pancytopenia, esp when given w/ gangciclovir. Both have mech of affecting DNA synth in hematopoietic stem cell lines.

180
Q

Folic or B12 more common in alcoholics?

A

Folic. Larger B12 stores.

181
Q

CO binding to heme - type of binding?

A

Competitive - and thus reversible it is NOT covalent

182
Q

Southern, Northern, Western blot

A

Southern - DNA, Northern -RNA Western - Protein

183
Q

Cyanide poisoning presentation.

A

Cyanide binds to iron containing enzymes (commonly cytochrome enzymes - CANT DO OXIDATIVE PHOSPHRYLATION) - can present as flushing, tachypnea, headache, tachyardia. Eventually leads to respiratoy distress and cardiac dysfunction. MAY LOOK LIKE CO POISONING.

184
Q

Treatment for cyanide poisoning. How does this work?

A

Nitrites (amyl nitrite) or Sodium thiosulfate. Nitrates. Nitrites cause Heme to bind Cyanide and sequesters it as methemoglobin. This cant carry O2 but at least you dont die. Alternatively Sodium thiosulfate binds to cyanide to form thiocyanide, which is less toxic and can be excreted in urine

185
Q

Kozak sequence - relation to AUG and disease?

A

Kozak is just upstream of AUG and related to initiate translation -mutation is related to B thalassemia .

186
Q

PI3K, PTEN, AKt, mTOR, PT system related to? What does end effect mTOR do?

A

anti-apoptosis. If you INC activity of this, then you get CA problems. mTOR leads to cell growth, prolif, survival etc in nucleus (aka anti-apoptotic)

187
Q

In sickle cells hen do you see fibrosis and atrophy and when do you see splenic congestion?

A

Congestion when younger. By young adulthood - fibrosis and atrophy - eventually leading to autosplenectomy (watch out for encapsulated bacteria)

188
Q

Chronic hemolytic anemia (Seen in SS), can predispose to?

A

folic acid deficiency due to constant erythrocyte turnover - macrocytic changes

189
Q

In pt w/ hemophilia, addition of what factor will lead to coagulation other than their deficiencies?

A

Thrombin! Its what they are trying to create

190
Q

Urokinase mech?

A

Same as tPA, INC plasminogen activation to plasmin (which cause cleavage)

191
Q

In heme preparation rproblem, what could ab pain and neurological symptoms + dark urine upon standing be attributed to?

A

Acute intermittent prophyria - due to prophobilinogen deaminase problem - Accumulated ALA. Tx w/ ALA synthase inibhitor.

192
Q

What lab findings are seen w F10 inhibitors

A

INC PT, PTT, normal TT. (as oppose to heparin and direct thrombin inhibitors (argatroban,bival) which actually inhibits TT (AT3 activit is 2.7,9,10?)

193
Q

HUS usu gotten from eaten what? Other food diarrheal association? Mayo/Custard, Oysters, Eggs, CHicken, canned food

A

Undercooked beef w/ E. coli O157:H7. Mayo/custards - staph A. Oysters - Vibrio, eggs/chicken - salmonella, canned food - botulinum

194
Q

Difference between unfractionated heparin and LMWHeparin? Name a specific LMWH?

A

Both contain polysaccharide that can bind to anti-thrombin. Howeve, unfractionated is longer and can bind to both anti-thrombin AND THROMBIN. This is not possible w/ LMWH. Enoxaparin is a LMWH.

195
Q

Hereditary spherocytosis - more likely to see auto-splenectomy or pigmented gallstones?

A

Pigmented gallstones. HS can lead to removal of RBC by spleen and INC levels of Unconj BIli -> pigmented gallstones. ALthough tx of HS is splenectomy, when you think autosplenectomy think sickle cell

196
Q

When is thrombin time dec?

A

When thrombin does work or DEC levels of fibrinogen

197
Q

Platelet drived growth fator recptor implicated in which leukemia?

A

Chronic myelomonocytic leukemia

198
Q

Epidermal growth factor receptor assoc w/ what CA?

A

Non-small cell lung CA, breast CA (HER2/neu), some ovarian/gastric tunors

199
Q

How does the PaO2 change with CO poisoning? Does this affect methemoglobin

A

PaO2 does not change. Carboxyhemoglobin around40%.

200
Q

What are causes of methemoglobin

A

Drugs (e.g. dapsone, nitrites), enzymes deficiencies, hemogklobinopathies

201
Q

What could splenomegaly, fever, sore throat, and cervical lymphadenopathy be?

A

Infectous mononucleosis

202
Q

What is CD14 for? What expresses it?

A

For co-receptor for LPS detection. On mostly monocytes and macrophages (probably dont need to know very little on N! and dendritic cells)

203
Q

If malaria is known to be in a region of chloroquine resistance, what do you treat with?

A

mefloquine

204
Q

Why is HbS more severe than HbC?

A

Hbs allows HYDROPHOBIC interactiosn among Hb molecules

205
Q

Speeds of hemoglobin moving through gel towards + anode?

A

Hemoglobin A > S > C. Because S has a nonpolar, and C is even less negative charge.

206
Q

1 year old kid with recurrent lower respiratory infection/pneumonia. Responds to candida injection. What does he have? Inheritance?

A

Bruton’s agammaglobulinemia - X linked immunodeficiency. Responds to candida so he still has T cells. His LN probably lack Germinal Centers.

207
Q

When do erythrocytes lose ability to synthesize heme?

A

When dthey lose their mitochondria - required for the first and final 3 steps of heme synth. 1st (Succinyl CoA+Glyicine (and ALAS), as well as Last - Ferrochelatase)

208
Q

Rat poison. What does it contain. What does ingestion do. What is to treatmetn

A

Brodifacoum, a long acting 4-hydroxycoumarin (VIT K ANTAGONIST ANTICOAGULANT) Present w/ coagulopathy and bleeding. Immediate treatmetn w/ FFP and VitK

209
Q

What does cryopercipitate contain?

A

F8, 13, vWF, fibrinogen (not vit K dependent factors)

210
Q

Syrup of ipecac. used for?

A

Emetic - use immediately after ingestion.

211
Q

What do you give preg woman w DVT? Heparin, Apsirin, Clopidogrel?

A

Heparin. Non-teratogeninc. Aspirin and Clopidogrel are not strong enough to independently treat DVT

212
Q

flat nasal bdrige, small mouth, low-set ears. Presentation of?

A

Downs T21.

213
Q

When do you see macroorchidism in pubertal boys?

A

Fragile X syndrome

214
Q

Degeneration of the central retina - think what? Tx?

A

Age related macular degeneration . anti-VEGF. Can see gray subretinal membrane

215
Q

Cataract - Where does it affect the eye? Presentation

A

Opacification of the lens. Loss of central vision

216
Q

Glaucoma - where does it affect the eye. Presentation?

A

Open ange (trabecular meshwork), closed angle - lens pushes against iris. Loss of peripheral vision

217
Q

Dry vs Wet AMD. Relationship?

A

Wet - presents w/ neovascularization, gray subretinal membrane. Dry - gradual vision loss in one or both eye - often progresses to wet (which is more common)

218
Q

What does folate deficiecny inhibit. How can you get past this? When would this be used?

A

Folate deficiency Inhibits formation of deoxythymidine monophosphate (dTMP), which liimits DNA synth. Can supplement w/ thymidine to INC dTMP levels. Can be used to reduce erythroprecrusor cell apoptosis

219
Q

When can you see INC HbF (a2g2) levels in adult? What is the molecular problem w/ B-thalassemia? Does Iron supplementation help?

A

B-thalassemia. mRNA processing (not protein folding). Iron supp does NOT help as they are not deificent

220
Q

alpha1 antitrypsin - what is the problem on the molecular level?

A

Protein folding error in Z mutation. (PiZZ - autosomal dominant problem)

221
Q

When does HbF swing over to HbA in infants?

A

Replaced during the first 6 months of life.

222
Q

Acute Leukemia - blasts?

A

20% blasts IN BONE MARROW (or peripheral blood) - So blood slide does not have to look liek 20%

223
Q

Very large blue cells. Think?

A

Acute Leukemia

224
Q

Erythemia infectiosum?

A

5th disease. Parvovirus - nonencapsuled single DNA - smallest DNA virus.

225
Q

Erythema subitum

A

6th disease - Roseola. Think subitum means quick - 3 days fever.

226
Q

Which ab can cross mom to baby?

A

IgG can cross. IgM is tgoo large to cross.

227
Q

APML (M3 AML) presentation?

A

Persistent infection and coagulopathy , hemorrhagic signs.

228
Q

Schilling test

A

Used to identify cauise of B12 def. Radioidentified B12. See if IF problem (give supplement), or Ileal diasease.

229
Q

Chronic low volume GI bleed preesnts as what kind of anemia?

A

hypochromic microcytic iron deficiency anemia.

230
Q

2,3 BPG - how is it produced and why what?

A

Produced by RBC. 1,3 BPG is taken from glycoolysis cycle and made by BISPHOSPHOGLYCERATE MUTASE into 2,3BPG

231
Q

What exactly does the JAK2 mutation do in myeloproliferative disease?

A

Makes hematopoietic stem cells more senstiive to growth factors

232
Q

When is extramedulalry hematopoiesis seen?

A

With severe chronic hemolytic anemias, such as B-thal

233
Q

Cyanocobalamin is?

A

artificial injections B12 - often presceribed in gastric bypass

234
Q

HMP shunt - what is it for? What enzymes are seen in it?

A

HMP shutn for nonoxidative reactions. Transketolase and transaldolase. This is how cells can synthesize RIBOSE FROM F6P.

235
Q

In all of bile processing, what is active/energy dependent?

A

The secretion of direct bilirubin is active. Indirect bilirubin uptake is passive.

236
Q

What bile is NOT water soluble. What is soluble

A

Unconjungated is insoluble. Conjugated is water soluble. Free excreted in urine

237
Q

Where is F8 synthesized and stored?

A

Synth in liver. Store din endothelium. DDAVP release vwF and F8 from endothelium.

238
Q

Desmopressin (DDAVP) work s on endothelial or platelets in vWD?

A

Although vWF in both endothelials and platelets, it realyl works on endothelial, which have both F8 and vWF.

239
Q

What happens if you treat B12 def w/ Folate?

A

ACTUALLY MAKES IT WORSE (more neuro problems)

240
Q

Relation between phenytoin and folate?

A

Phenytoin can cause low folate levels. On the flip side, high dose folate can lead to antagonization of phenytoin, which can lead to seizure in high risk pt.

241
Q

G6PD in what 2 important pathways?

A

Glyoclysis and Pentose Phosphate pathway -(NADPH formation)

242
Q

What can trigger G6PD Deficiency hemolytic anemia?

A

TMP-SMX, bactrim, dapsone, antimalarials, nitrates, infections, fava beans (other oxidants)

243
Q

What are serum ferritin and transferrin levels in menorrhagia induced anemia?

A

Serum ferritin is low, transferrin is high (trying to suck stuff up) - If chronic, MCV is microcytic, hypochromic

244
Q

Iron deficiency? Commonly from?

A

Diet or heavy menses. Low ferritin. Menorrhagia

245
Q

vWF D in woman - can present as?

A

Various bleeding, esp heavy menstrual periods and nosebleeds. Due to vWF and F8 problem.

246
Q

What type of Hb is elevated in B thalassemia in adult?

A

HbA2

247
Q

What drugs INC warfarin potency, and what drugs DEC warfarin potency. How?

A

Warfarin broken down by p450. Cimetidine, amiodarone and TMP-SMX INC warfarin potency by inhibiting metabolism (p450). Rifampicin, phenobarbital and phenytoin ENHANCE p450 and thus DEC warfarins effect. Cholestyramine binds warfarin and other drugs in intestine and also DEC therapeutic effect (remember warfarin is oral)

248
Q

How does pregnancy affect nephron function? Where?

A

DEC reabs in of glucose and amino acids PCT -> glucosuria and aminaciduria

249
Q

Hartnup disease - inheritance? Defect? Treatment?

A

AR - neutral amino acid transporter (tryptophan) defect in PCT. Leads to neutral aminoaciduria and DEC absorption in gut (problem there too). Results in pellagra like symtpoms - Tx w/ high protein diet and nicotinic acid.

250
Q

Causes of Calcium Kidney stones. Treatment?

A

Hypercalciruia (most are normocalcemia). Ethylene glycol (antifreeze), vitC abuse, Crohn disease. Tx - Thiazide an citrate

251
Q

Considerations of Ammonium magnesium phosphate?

A

Urease + bugs (prteus, staphylococcus, Klebsiella). Urine is alkaline. Can form staghorn calculi and be nidus for UTI.

252
Q

Uric acid crystal and Cystine crystal - treatment?

A

Alkalinize urine

253
Q

Where does Renal Cell CA originate from? Where does it metastasize to?

A

Proximal tubule cells -> clear cells filled w/ lipids/carbs. Lungs and Bone.

254
Q

Renal oncocytoma - Benign/CA?

A

Benign epithelial cell - well circumscribed mass w/ central scar. Large eosinophilic cells w/ abundant mitochondria w/o perinuclear clearing (opposite of Renal Clear Cell CA).

255
Q

Risk factors for Transitional Cell CA? mnemonic?

A

P SAC. Phenacetin, Smoking, Aniline dyes, Cyclophosphamide.

256
Q

During severe hypotension, what does GFR, RPF, and FF look like?

A

GFR is Dec, RPF is DEC! and FF is INC. So GFR is still DEC in hypotension. Compensation of AT2 on efferent is not enough

257
Q

How does filtered K serum flow in the nephron as a percentage of the total filtered K.

A

PCT 65% left, Ascending Henle - 5-10% left. At DCT, 100% SECRETED. So it’s first all absorbed, then secreted!

258
Q

Uric acid stones in a patient being treated for CA?

A

THink tumor lysis syndrome. (rlease K, phosphorous, uric acid). Must prevent by alkalizing and hydrating urine. High urine flow and high pH prevents precipitation.

259
Q

Where does Uric acid stone precipitation occur?

A

In the collecting ducts! THis is due to low urine pH. Collecting Duct is usually the spot w/ the lowest H.

260
Q

NSAID associated chronic renal injury is?

A

Renal Papillary Necrosis and Chronic Interstitial Nephritis.

261
Q

When they give you all the numbers, may be worth trying out winters formula (give here) to see if compensation is correct

A

1.4xbicarb +8 (+-2)

262
Q

Name 3 trinucleotide repeat mutations

A

Myotonic dystrophy, fragile X syndrome, Huntington disease

263
Q

VIsual Impairments in HIV patients. Think what? What is treatment? What is tox of treatment?

A

CMV induced retinitis. Treatment includes ganciclovir, foscarnet, cidofovirGanciclovir tox - Each one of Pancytopenia + carginogen, teratogen, mutagen, inhibits spermatogenesis (vs acyclovir has nephrotox!), Foscarnet tox - Pyrophosphate analog that chelates Calcium - induces Mg wasting and DEC parathyroid hormone (both hypoMg and Ca - both of these can promote SEIZURES)

264
Q

Treatment of CMV that can induce seizures. Mechanism?

A

FOscarnet - Ca chelator. Can induce both hypoMg and hypoCa, which promote Seizure. Promotes Mg waisting and DEC PTH

265
Q

THiazide diuretcs can induce 4 metabolic states

A

Hypokalemia, metabolic alkalosis, hyponatremia, hyperCa

266
Q

Torsemide is a ? Along with 3 others

A

Loop diuretic. FUrosemide, Torsemide, Bumentanide, Ethacrynic acid

267
Q

PSGN has what kind of deposits?

A

Suepithelial lumpy bumpy

268
Q

Aldosterone promotes loss 2 serum electrolytes

A

K and H

269
Q

What are glucose levels in the nephron?

A

FIltered then completely reabs in PCT (in normal states)

270
Q

What are 3 alpha adrenergic ANTAGONISTS. What are their effects on BPH?

A

Terazosin, Tamsulosin, Prazosin. These DEC tone (Rela smooth muscle) allowing for flow. They do NOT reduce volume of prostate

271
Q

What drug do you give when you are trying to DEC SIZE of prostate? Name 2 drugs

A

5-a reducatase inhibitors - finasteride, dutasteride

272
Q

ATN. Walk through 3 phases. What are the concerns for each phase?

A

Phase 1 Initiation - acute ischemiaPhase 2 - DEC in output, INC Cr/BUN, hyperkalemiaPhase 3 - Gradual INC in urine output leading to high volume diuresis - may lead to HYPOK, Mg, PO4 and Ca. Hypokalemia is feared complication due to high volume hypotonic urine.

273
Q

In the kidney, think of H2PO4 as? What else is in this same category?

A

Titratable acid (HPO4 + H) - excreted in acidosis (DKA etc) . NH3 is also a titratable acid. Allows for the excretion of more acid in urine without FURTHER DEC pH.

274
Q

When would you see Uracil or other RNA in DNA?

A

Primase - DNA depednent RNA polymerase

275
Q

DNA polymerase 3 vs 1

A

3 is primary enzyme for synthesizing daughter DNA strands - DNA polymerase 1 functions to replace RNA primers (Set by Primase) w/ DNA.

276
Q

Multiple oxalate crystals. Think what?

A

Ethylene glycol. Metabolized to glcolic acid in GI, which is toxic to renals and then becomes oxalic acid and precipitates Ca. Oliguria, anorexia, flank pain are characteristic after ethylene glycol poisoning 24-72 hours after ingestion. See IN anion gap metabolic acidosis, INC osmolar gap, and stones

277
Q

Where are the deposits in PSGN and Membranous neprhopathy?

A

Subepithelial

278
Q

What is immunohistochemistry stain for nephritis?

A

SILVER methenamine

279
Q

How is early screening for diabetic nephropathy performed?

A

Screen for microalbuminuria (30-300 mg/day)

280
Q

When does acute rejection occur, what is mediating the damage, and what is seen on histopathology? Treatment?

A

Occurs within week os transplantation - mediated by HOST T cells that act against MHC antigens. Histopath - mononuclear infiltrate. Tx - calcineurin inhibitors and systemic corticosteroids

281
Q

Metabolic/physiological parameters seen with aspirin(acute salicylate intox) OD.

A

Respiratory alkalosis is right after ingestion via medullary respiratory center. Few hours in, anion gap metabolic acidosis develops - At high doses - uncouple oxidative phosphorylation, inhibit TCA cycle, accumulation of metabolic intermediates like ketoacids, lactate, pyruvate.

282
Q

Heart failure patient - what diuretic should you give?

A

Spironolactone. ALthough furosemie is stronger, spironolactone shwn to work better in evidence based RALES trial. likely due to neurohormonal effects of aldosterone inhibition -> DEC ventricular remodeling and DEC cardiac fibrosis

283
Q

How can acute rejection present? What is the host response? How to treat acute rejection (2 drugs)?

A

Feaver, chills, malaise, arthralias, INC serum creatinine, HTN, reduced urine output. can be Ab-mediated OR Cell mediated (see in interstitium/pareynchyma) Tx w/ prednisone and tacrolimus

284
Q

Mononuclear cell w/ IL2 receptor and MHC2 receptor? How can you target this cell

A

T cell . Anti-CD3 antibody

285
Q

Anti-EGFR (epidermal growth factor receptor) - Examples of drugs and used for what?

A

Cetuximab, used for non-small cell lung CA, colorectal, pancreatic and squamous cell CA of head and neck. `

286
Q

Anti-VEG ab - example and used for what?

A

Bevacizumab - used to tx metastatic colon, nonsmall cell lung, renal cell CA and recurrent gliobastoma multiforme

287
Q

What are Mononuclear leukocytes? Also known as?

A

AKA agranulocytes. Lymphocytes (including NKTcells) and monocytes.

USMLE (16 decks)

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