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Lecture 25+26 Flashcards

1
Q

Type IIB Familial combined hyperlipidemia

A

high LDL and high VLDL

Overproduction of VLDL by liver

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2
Q

Type IV Familial hypertriglyceridemia

A

high VLDL

Overproduction and/or impaired catabolism of
VLDL

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3
Q

Type I Familial hyperchylomicronemia

A

increase in chylomicrons

deficiency in LPL or ApoCII

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4
Q

Type IIA Familial hypercholesterolemia

A

high LDL

Decreased or no functional LDL receptor
expression

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5
Q

Type III Familial dysbetalipoproteinemia

A

high IDL

Abnormal apoE

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6
Q

Type V Familial mixed hypertriglyceridemia

A

increase in chylomicrons and high VLDL

Increased production or decreased clearance of
VLDL & chylomicrons.

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7
Q

MOA of statins

A

Statins are competitive inhibitors of HMG-CoA reductase, the enzyme that catalyzes the first committed step of cholesterol biosynthesis

By inhibiting cholesterol synthesis statins
deplete intracellular supply of cholesterol

Depletion of intracellular cholesterol leads to
upregulation of HMG-CoA reductase, and upregulation
of the LDL receptor

Upregulation of LDL receptors results in increased clearance of LDL from the blood

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8
Q

The uses of statins

A

• Drugs of choice for LDL reduction.
• Reduce cardiovascular mortality.
• Lower LDL levels in all types of hyperlipidemias.
• Homozygotes for familial hypercholesterolemia
lack functional LDL receptors and thus benefit much less from treatment with statins.
• Contraindicated in pregnancy

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9
Q

AE of statins

A

Elevation of aminotransferases

Myopathy and rhabdomyolysis

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10
Q

Niacin

A

Decreases VLDL, LDL and Lp(a) levels.

It increases HDL levels

Most effective agent for increasing HDL and the only agent that may reduce Lp(a).

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11
Q

MOA of niacin

A

Niacin inhibits adenylyl cyclase in adipocytes. Leading to inhibition of hormone-sensitive lipase

In the liver niacin inhibits synthesis and
esterification of fatty acids. VLDL production is
decreased

increases LPL activity

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12
Q

uses of Niacin

A

• Niacin is the most effective drug for raising HDL.
• Particularly useful in patients with combined
hyperlipidemia and low HDL levels.
• Effective in combination with statins

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13
Q

AE of niacin

A

Intense cutaneous flush after each dose of niacin when the drug is started or the dose increased

taking aspirin before will decrease the flushing

Pruritus, rashes, dry skin.
Acanthosis nigricans.
Nausea and abdominal discomfort
hepatotoxicity 
hyperglycemia 
elevate uric acid levels
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14
Q

Fibrates examples

A

Gemfibrozil
Fenofibrate

Fibrates lower VLDL levels and increase HDL
levels

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15
Q

MOA of fibrates

A

Fibrates activate peroxisome proliferator activated receptor-alpha (PPAR-alpha).
• PPAR-alpha receptors are expressed primarily in
liver and brown adipose tissue.
• Activation of PPAR-α by fibrates leads to a decrease in plasma TG levels and increase in plasma HDL levels due to the increase LPL and decreased expression of apoC-III

increase HDL and decrease TG

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16
Q

uses for the fibrates

A

DOC in severe hypertriglyceridemia

Reasonable consideration in moderate
hypertriglyceridemia.

As monotherapy, fibrates offer the highest TG reduction, followed by niacin, W-3-fatty acids, statins, and ezetimibe.

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17
Q

AE of fibrates

A

Mild GI disturbances.
Myositis
Lithiasis

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18
Q

drug interactions with fibrates

A

Gemfibrozil inhibits hepatic uptake of statins, thus more statin in blood
(Gemfibrozil competes for the glucuronosyl transferases that metabolize most statins)

increased risk for rhabdomyolysis

fenofibrate does not interfere with interact with statin metabolism

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19
Q

bile acid binding resins

A

Cholestyramine
Colestipol
Colesevelam

Useful only in hyperlipidemias involving isolated
increases in LDL

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20
Q

MOA of bile acid binding resins

A

Bind to anionic bile acids in the intestinal lumen and prevent their reabsorption.

The resin-bile acid complex is excreted in the feces, thus preventing bile acids from returning to the liver by the enterohepatic circulation

The reduction in bile acid concentration causes
hepatocytes to increase conversion of cholesterol
to bile acids. This leads to up-regulation of LDL receptors in the liver

decrease in LDL levels
modest increase in HDL
increase synthesis of cholesterol

21
Q

uses of bile acid binding resins

A

Used with statins or niacin to increase LDL
reduction.

Drugs of choice for pregnant women and for
children.

Little effect in individuals who completely lack
functional LDL receptors

22
Q

AE of bile acid binding resins

A

GI adverse effects: bloating, nausea, cramping
and constipation.
Colesevelam produces fewer GI adverse effects
than cholestyramine or colestipol.

They may increase TG: contraindicated in
hypertryglyceridemia

23
Q

bile acid binding resins: drugs interactions

A

Cholestyramine and colestipol reduce absorption

of several drugs and liposoluble vitamins

24
Q

Ezetimibe

A

cholesterol absorption inhibitor

Inhibits intestinal absorption of cholesterol and
phytosterols.

Its primary clinical effect is to lower LDL

25
MOA of ezetimibe
Ezetimibe inhibits an intestinal transport protein (NPC1L1), which takes up cholesterol from the lumen This triggers a compensatory increase in cholesterol synthesis (which can be inhibited with a statin). upregulation of LDL receptors, which enhances LDL clearance from plasma
26
uses of Ezetimibe
Useful in combination with a statin in patients unable to reach their LDL goal on statin monotherapy. First non-statin drug that should be considered as an adjunct to a statin. Ezetimibe is only used as monotherapy in patients who do not tolerate statins.
27
AE of ezetimibe
Low incidence of reversible impaired hepatic function. Small increase in incidence when ezetimibe is given with a statin. Myositis has been reported rarely
28
ezetimibe drug interactions
Bile-acid sequestrants inhibit absorption of ezetimibe. The two agents should not be administered together
29
Hypertension- Nephrosclerosis
associated with sclerosis of renal arterioles and small arteries; it is strongly associated with hypertension patho: Medial and intimal thickening, a response to hemodynamic changes, aging, genetic defects Hyalinization of arteriolar walls, caused by extravasation of plasma proteins through injured endothelium and by increased deposition of basement membrane matrix
30
Benign Nephrosclerosis
vascular: Medial and intimal thickening Hyaline arteriolosclerosis glomerular: Global sclerosis FSGS – compensatory hyperfiltration due to nephron loss tubulointerstitial: Tubular atrophy Ischemia mediated interstitial fibrosis
31
patho of benign nephrosclerosis
hypertension = medial and intimal thickening (arteries) | = luminal narrowing = ischemic injury and decreases pressure transmission
32
histo of benign nephrosclerosis
gross: Cortical surfaces have a fine, even granularity that resembles grain leather Loss of mass is due mainly to cortical scarring and shrinking histo: Hyaline arteriosclerosis Microscopic subcapsular scars with sclerotic glomeruli and tubular dropout, alternating with better preserved parenchyma
33
CF of benign nephrosclerosis
* Long-standing history of hypertension * Slowly progressive elevation in serum Creatinine * Mild proteinuria (<1 g/day) * No microscopic hematuria * Few progressing to ESRD * Clinically: long-standing hypertension * Bland urine sediment with mild proteinuria
34
Malignant Nephrosclerosis
hypertension (malignant HPN) | organ damage and renal lesions
35
patho of malignant nephrosclerosis
HTN = Medial and intimal thickening and Duplication of BM = luminal narrowing = ischemic injury and fibrinoid necrosis in severe HTN
36
Renal Artery Stenosis
hypertension secondary to renal artery stenosis is caused by increased production of renin from the ischemic kidney Ischemic kidney is reduced in size and shows signs of diffuse ischemic atrophy Crowded glomeruli, atrophic tubules, interstitial fibrosis, and focal inflammatory infiltrates mild arteriosclerosis
37
CF of renal artery stenosis
Sudden onset of uncontrolled HTN in previously well controlled patient Accelerated/ malignant hypertension Intermittent pulmonary edema with normal LV function Elevated plasma or renal vein renin Fibromuscular dysplasia
38
Thrombotic Microangiopathies (TMA)
refers to lesions seen in various clinical syndromes characterized by microvascular thrombosis accompanied by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure first: known etiology Shiga toxin mediated hemolytic uremic syndrome (HUS and atypical HUS (complement mediated TMA) Thrombotic thrombocytopenic purpura (TTP) secondary: develop in the background of other diseases or conditions without well-defined etiology like malignant hypertension and scleroderma associated TMA
39
hemolytic uremic syndrome (HUS)
Caused by diverse insults that lead to thrombi in capillaries and/ or arterioles in various tissue beds, including those of the kidney 1. Flow abnormalities → shear and mechanically damage red cells → microangiopathic hemolytic anemia (MAHA) 2. Microvascular occlusions that cause tissue ischemia and organ dysfunction 3. Widespread “consumption” of platelets lead to thrombocytopenia usually seen in children and caused by enterohemorrhagic E.coli More severe renal failure, less pronounced CNS involvement Associated with other infections: viral, Shigella, Salmonella Drug-induced: Quinine (tonic water), Gemcitabine, Cyclosporine, Ticlopidine, Oral contraceptives
40
histo of Thrombotic Microangiopathies
``` Microangiopathic hemolytic anemia Thrombocytopenia Purpuric rash Acute renal failure fever, headache ```
41
Thrombotic thrombocytopenic purpura (TTP)
CNS involvement more pronounced, renal failure less severe Often associated with SLE, HIV, hematological malignancy
42
AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE
Hereditary disorder characterized by multiple expanding cysts of both kidneys that ultimately destroy the renal parenchyma and cause renal failure clinically silent; manifests in adulthood can be the PKD1 gene or PKD2 gene encodes polycystin 1 and 2 PKD2 is milder
43
CF is AD polycystic kidney disease
asymptomatic until 40s and 50s Incidentally diagnosed due to work up form hypertension, abdominal mass, flank or back pain Renal failure, cardiovascular and infections- common causes of death
44
manifestations due to cyst formation
``` HTN hematuria flank pain Nephrolithiasis Gram negative infection ``` hepatic cysts
45
AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE
Manifests in neonates, infants and children Mutation in PKHD1 gene on chromosome 6p21 coding for fibrocystin protein Kidney is enlarged with a smooth external surface Dilated elongated channels are present at right angles to the cortical surface, completely replacing the medulla and cortex Congenital hepatic fibrosis Renal failure and death may occur in infants
46
MEDULLARY SPONGE KIDNEY
* Multiple cystic dilations of the collecting ducts in the medulla * Occurs in adults * Unknown etiopathogenesis * Usually discovered radiographically * Renal function is usually normal
47
SIMPLE CYSTS
* Can be single or multiple * Common postmortem findings without clinical significance * More common with older age
48
Alport Syndrome
inherited disease of the basement membrane collagen type IV which is crucial for normal function of the lens, cochlea, and glomerulus most commonly X linked genes coding for the alpha chains in collagen type IV → COL4A4 and COL4A5 defective assembly of the collagen network → defect in GBM usually males 5-20 years gross or microscopic hematuria along with red cell casts Other features: nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy
49
path features of alport syndrome
GBM shows irregular foci of thickening alternating with attenuation (thinning) Pronounced splitting and lamination of the lamina densa, often producing a distinctive “basket weave appearance” Immunohistochemistry with antibodies against alpha chains- negative in basement membranes With progression of disease, focal and diffuse glomerulosclerosis sets in

CRS (16 decks)

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