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CRS > Lecture 5+6+DLA > Flashcards

Lecture 5+6+DLA Flashcards

1
Q

edematous states

A

increased NaCl reabsorption → water retention & blood
volume

ex: 
HF
hepatic ascites
nephrotic syndrome 
premenstrual edema
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2
Q

non-edematous states

A

hypertension
hypercalcemia
diabetes insipidus

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3
Q

diuretics

A

Inhibitors of renal ion transporters that decrease the
reabsorption of Na+ at different sites in the nephron
(natriuretics)

used:
managing abnormal fluid retention
hypertension

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4
Q

site of action of CA inhibitors

A

proximal tubule (reabsorption of water, K, and Na/ secretion of organic acid and base secreting systems

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5
Q

site of action of thiazides

A

distal convoluted tubule (reabsorption of Cl and Na)

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6
Q

site of action of the K sparing and ADH antagonists?

A

collecting duct (reabsorption of Na and water / secretion of H and K)

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7
Q

site of action of loop diuretics

A

thick ascending loop of henle (reabsorption of Na, K, and Cl also Ca and Mg)

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8
Q

loop diuretics

A

furosemide

Highest efficacy in removing Na+ & Cl from body
Act on ascending limb of Loop of Henle

applications:
managing edema associated with HF, hepatic, and renal disease
moderate to severe hypertension

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9
Q

MOA of loop diuretics

A

act on the ascending limb of loop of henle

Block NKCC2 Na+ /Cl- /K+ cotransporter

more Na, K, and Cl in tubular fluid = more water excretion

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10
Q

actions of loop diuretics

A
  • Increased urine output
  • Increased K+ excretion
  • Increased Ca2+ excretion
  • Increased Mg2+ excretion
  • Increased prostaglandin synthesis
  • Decreased renal vascular resistance
  • Increased renal blood flow
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11
Q

adverse effects of loop diuretics

A
  • Ototoxicity
  • Hyperuricemia
  • Acute hypovolemia
  • Hypokalemia
  • Hypomagnesemia
  • Allergic reactions
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12
Q

clinical applications of thiazides?

A

hypertension
HF (mild-mod)
hypercalciuria (useful for kidney stones)

diabetes insipidus
premenstrual edema

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13
Q

examples of thiazides

A

Hydrochlorothiazide

Chlorthalidone (longest duration)

Metolazone (most potent)

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14
Q

MOA of thiazides

A

act at the distal convoluted tubule
block the NCCT Na/Cl transporter

more Na and Cl in tubular fluid
more water excretion

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15
Q

actions of the thiazides

A
  • Increased Na+ & Cl- excretion
  • Increased K+ excretion
  • Increased Mg2+ excretion
  • Decreased urinary Ca2+ excretion
  • Decreased peripheral vascular resistance
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16
Q

adverse of thiazides

A

Hypokalemia • Hyponatremia • Hyperuricemia • Hyperglycemia • Hyperlipidemia • Hypersensitivity • Sexual dysfunction

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17
Q

K sparing examples (aldosterone)

A

Aldosterone antagonists:

Spironolactone and Eplerenone

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18
Q

when to use K sparing? (aldo antagonist)

A

act at the collecting tubule
used when their is excess aldosterone

must monitor K closely

19
Q

clinical uses of K sparing ( aldo antagonist)

A

heart failure ( spironolactone)
hypertension
primary hyperaldosteronism
edema

20
Q

K sparing MOA (aldo antagonist)

A

act act the collecting tubule

Antagonize aldosterone at intracellular cytoplasmic
receptor sites (no transcription)

less Na reabsorption and decreased K excretion

21
Q

adverse effects of K sparing

A

aldosterone antagonists

Gastric upset & peptic ulcers

Endocrine effects (antiandrogen)

Hyperkalemia

Nausea, lethargy, mental confusion (rare)

22
Q

K sparing Na channel inhibitors

A

Amiloride and Triamterene

block the Na channels (less Na/K exchange)

23
Q

MOA of k sparing (Na channel inhibitors)

A

act on collecting tubule

Directly block epithelial sodium channel (ENaC) →
decreasing Na+ /K+ exchange

decreased Na+ reabsorption & K+ excretion

24
Q

AE of the K sparing (Na channel inhibitors)

A 
Hyperkalemia
Hyponatremia
Leg cramps
GI upset
Dizziness, pruritus, headache & minor visual changes
25
Q

CA inhibitors

A

Acetazolamide

act at the proximal tubular epithelial cells
less effective

26
Q

clinical app of CA inhibitors

A

Glaucoma
Epilepsy (used alone or with other antiepileptics)
Mountain sickness prophylaxis
Metabolic alkalosis

27
Q

MOA of CA inhibitors

A

Inhibits intracellular carbonic anhydrase

Decreases ability to exchange Na+ for H+

Decreases activity of Na+ /K+ ATPase (diuresis)

HCO3 - is retained in lumen (increasing urinary pH)

28
Q

AE of the CA inhibitors

A 
• Metabolic acidosis
• Hyponatremia
• Hypokalemia
• Crystalluria
• Malaise, fatigue, depression, headache, GI upset,
drowsiness, paresthesia
29
Q

Giant cell Arteritis

where? epi? patho? clinical?

A

Large Vessel Vasculitis
mostly seen in head and neck (temporal A)

epi:
seen in elderly; more common in women

patho:
T cell mediated response to an uncharacterised antigen in the vessel wall
Pro inflammatory cytokines like TNF (targets for treatment) (+/- Anti endothelial cell antibodies)

clinical features:
headache
facial and jaw pain
ocular symptoms

30
Q

micro of giant cell arteritis

A

Focal, nodular thickening with reduction of lumen due to intimal hyperplasia

Granulomatous inflammation of intima and inner media

Multinucleated giant cells

Fragmentation of internal elastic lamina

31
Q

Takayasu Arteritis

A

Large Vessel Vasculitis:

seen in aortic arch and great vessels, renal, and vertebral A.

epi:
young women

patho:
unknown maybe autoimmune

features:
pulses are weaker or absent in affected vessels
ocular and neurological symptoms

32
Q

histology of takayasu arteritis

A

Destruction and collagenous fibrosis of the arterial media associated with mononuclear infiltrates and inflammatory giant cells

33
Q

Polyarteritis Nodosa

A

Medium Vessel Vasculitis

involved:
Medium sized arteries of kidney > heart > liver > gastrointestinal tract (Lungs are spared)

epi:
seen in young adults

patho:
Immune complex mediated damage following Hepatitis B (some are unknown)

clinical:
Kidney: hypertension, hemorrhage, infarction
Heart: myocardial infarction, pericarditis, heart failure
Liver and GIT: abdominal pain, mesenteric ischemia and infarcts
Rashes, gangrene, peripheral neuropathy

34
Q

histo of polyarteritis nodosa

A

transmural inflammation
fibrinoid necrosis
patchy involvement

35
Q

Kawasaki Disease

A

medium vessel

coronary arteries are mainly involved

epi:
cardiac disease in kids

patho:
Delayed hypersensitivity reaction to newly uncovered vascular antigens (autoantibodies)

clinical: 
Fever
Cervical lymphadenopathy
Conjunctival and oral erythema
"Strawberry Tongue”
Blistering
Edema of hands and feet /Erythema of palms and soles
Desquamative rash
Coronary arteritis and aneurysm rupture and hemorrhage
MI
36
Q

histo of Kawasaki disease

A

transmural necrotizing inflammation
acute inflammatory cells
less fibrinoid necrosis
can have superimposed aneurysm/thrombosis

37
Q

Buerger Disease

A

medium vessel

tibial and radial arteries are involved

epi:
young male smokers (less than 40)

patho:
Smoking tobacco- direct endothelial injury → inflammation and thrombosis

clinical:
• Raynaud phenomenon and cold sensitivity
• Instep foot pain induced by exercise (instep claudication)
• Superficial nodular phlebitis (venous inflammation)
• Rest pain due to neural involvement

38
Q

histo of buerger disease

A

thrombus that has microabcesses of neutrophils and INF

occlusion of the vessel

39
Q

Granulomatosis with polyangiitis

A

small vessel

triad: necrotizing granulomas of the upper and lower respiratory or both
epi: middle aged; more common in men
patho: c-ANCA/ PR3-ANCA mediated

clinical: 
• Sinusitis, pneumonitis; Hemoptysis
• Mucosal ulcerations
• Hematuria
• Rashes, myalgia, neuritis
40
Q

histo of Granulomatosis with polyangiitis

A

Ulcerative lesions surrounded by granulomas with geographic necrosis and
accompanying vasculitis

Necrotizing granulomas are surrounded by a zone of proliferating fibroblasts with giant cells and leukocyte infiltrate

Respiratory tract: sinusitis, bilateral nodular infiltrates with cavitations

Kidney: crescentic glomerulonephritis

41
Q

Churg Strauss Syndrome

A

small vessel

patho:
p-ANCA/ MPOANCA mediated

epi:
really any age; slightly female more likely

clinical:
Respiratory tract- attacks of asthma; allergic rhinitis and sinusitis
• Skin- palpable purpura
• GIT- bleeding
• Kidney (uncommon as compared to other small vessel vasculitis)- hematuria and proteinuria
• Neuropathy, myocarditis and cardiomyopathy

42
Q

histo of Churg Strauss Syndrome

A

Pulmonary infiltrates on imaging
• Necrotizing granulomatous inflammation- both in vessel wall and extravascular
• Tissue eosinophilia as well as peripheral blood
eosinophilia
• Serology: raised IgE levels

43
Q

Microscopic Polyangiitis (MPA)

A

small vessel

epi:
50-60; more common in males

patho:
c-ANCA/ PR3-ANCA mediated

Antibody responses to antigens such as drugs (e.g., penicillin), microorganisms (e.g., streptococci), heterologous proteins, or tumor proteins

clinical: 
• Hemoptysis, hematuria and proteinuria
• Bowel pain or bleeding
• Muscle pain or weakness
• Palpable cutaneous purpura
44
Q

histo of MPA

A

Segmental fibrinoid necrosis of the media with focal transmural necrotizing lesions

No granulomas or eosinophils or nasopharyngeal involvement

neutrophils are seen

CRS (16 decks)

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