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BM213 Pharmacology > Block E > Flashcards

Block E Flashcards

1
Q

functions of kidneys

A

*-regulation of water and inorganic ion balance
-removal of metabolic waste products from blood and excretion in urine
-removal of foreign chemicals in the blood and excretion in urine
-gluconeogenisis

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2
Q

how many nephron in the kidneys

A

2.5million in the 2

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3
Q

nephron functional components

A

tubular component and vascular component

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4
Q

what does glomerular filtrate do

A

drains into bowman’s space and then into proximal convolutes tubule

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5
Q

how do endothelium allow small molecules through

A

they have pores

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6
Q

what does podocytes having a negative charge do

A

it along with the basement membrane stops proteins getting through into tubular fluid

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7
Q

what does JGA do

A

helps regulate renal blood flow, GFR and also indirectly modulates sodium balance and systemic BP

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8
Q

how do the kidneys reduce renal pressure

A

intrarenal redistribution of pressure and increased absorption of salt and water

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9
Q

what does a decreased pressure in renal arterioles and sympathetic activity lead to

A

renin and angiotensin II production

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10
Q

what does angiotensin II affect in the kidneys

A

causes direct constriction of renal arterioles. stimulation of aldosterone synthesis- sodium absorption and increase in intravascular blood volume

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11
Q

what is the principal factor controlling angiotensin II levels

A

renin release

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12
Q

decreased circulating volume stimulates renin release via

A

decreased BP, decreased salt, decreased renal perfusion pressure

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13
Q

what does aldosterone stimulate

A

sodium reabsorption and potassium excretion by the renal tubule

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14
Q

how does aldosterone exert indirect negative feedback on RAAS

A

by increasing ECV and lowering plasma (K+)

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15
Q

pharmacologic treatment of cardiovascular disease

A

directs, sympatholytics, calcium channel blockers, direct-acting vasodilators

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16
Q

classification of diuretics

A

all indirectly prevent the re-absorption of water in kidneys
loop diuretics- furosemide supplemented with spironolactone or amiloride
thiazides- bendroflumethiazide
potassium sparing diuretics- not acting directly on sodium channels

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17
Q

loop diuretics mechanism of action

A

inhibiting the Na/K/2cl co-transporter

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18
Q

thiazide diuretics mechanism of action

A

inhibit the sodium-chloride transporter in the distal tubule, because this transporter only reabsorbs 5% of filtered sodium these diuretics are less efficacious than loop in producing diuresis and natriuresis

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19
Q

liver function

A

-major role in protein, carbohydrate and lipid homeostasis
-stores glycogen, vitamins and iron
-contains an extensive reticuloendothelial system for the synthesis and breakdown of blood cells
-liver cells metabolise, detoxify and excrete both endogenous and exogenous compounds

20
Q

how are liver diseases identified

A

liver function tests (LFTs), complete blood count, CT scans, MRIs, ultrasounds, liver biopsy

21
Q

how are liver diseases managed

A

limiting alcohol, maintaining healthy weight, drinking more water

22
Q

how are liver diseases treated

A

hepatitis- antiviral drugs
liver inflammation- steroids
blood pressure medication
antibiotics

23
Q

how is hepatitis A spread

A

contact with contaminated food or water, symptoms may clear up without treatment, recovery a few weeks

24
Q

how is hepatitis B spread

A

can be acute or chronic, spread through bodily fluids, is treatable but no cure

25
Q

how is hepatitis C spread

A

can be acute or chronic, spread through contact with blood of someone with hepatitis C, often doesn’t cause symptoms in early stage but can lead to permanent liver damage

26
Q

what is hepatitis D

A

serious form of hepatitis that only develops in people with hepatitis B

27
Q

how is hepatitis E spread

A

by drinking contaminated water, generally clears up on its own in a few weeks without any lasting complications

28
Q

treating hepatitis

A

interferons- don’t directly kill viral or cancerous cells, they boost the immune system response stimulating T cells and other immune system cells to attack
anti-viral drugs- ombitsdvir with paritaprevir and ritonavir
sofosbuvir- inhibits the hepatitis C virus NS5B protein

29
Q

fatty liver disease

A

alcohol fatty liver disease, caused by heavy alcohol consumption
non-alcohol fatty liver disease, caused by unknown

30
Q

what happens if fatty liver diseases are left unmanaged

A

both types can cause liver damage, leading to cirrhosis and liver failure. diet and other lifestyle changes can often improve symptoms and reduce risk of complications

31
Q

pioglitazone

A

improves the sensitivity of hepatic tissue to insulin. they are synthetic ligands for PPARs, they alter the transcription of genes, influencing carbohydrate and lipid metabolism- resulting in changed amounts of protein synthesis and therefore metabolic changes

32
Q

autoimmune hepatisis

A

causes immune system to attack liver, causing inflammation. left untreated can lead to cirrhosis and liver failure

33
Q

primary biliary cirrhosis

A

results from damage to the bile ducts in liver, causing build up of bile. PBC can lead to cirrhosis and liver failure

34
Q

primary sclerosing cholangtis

A

infammatoru condition that causes gradual damage to bile ducts. they eventually become blocked, causing bile to build up in liver which can lead to cirrhosis or liver failure

35
Q

prednisolone

A

increases the concentration of neutrophils; decreases T&B lymphocytes, monocytes, eosinophils and basophils. decrease in cytokine release, including decrease in IL-2 and TNF alpha

36
Q

azathioprine (AZA)

A

immunosuppressive agent that acts through its effects as an antagonist of purine metabolism, resulting in the inhibition of DNA, RNA and protein synthesis

37
Q

liver cancers

A

first develop in liver. if cancer starts elsewhere then spreads to liver it’d called secondary liver cancer.
most common liver cancer= heptocellular carcinoma, tends to develop as several small spots of cancer in liver but can start as a single tumour also

38
Q

how are liver cancers treated

A

surgery, chemotherapy and pharmacotherapy

39
Q

mechanism of action of immune checkpoint inhibitors

A

two signals are required to initiate the activation of T cells. first signal involves the binding of a MHC to a TCR on T-cells. second signal arises with the binding of the APC ligands CD80 or CD86 to CD28 on T cells

40
Q

what is cholestasis

A

impairment of bile formation and/or bile flow, which may clinically present with fatigue, pruritus, dark urine, pale stools and in its most overt form jaundice and signs of fat soluble vitamin deficiencies

41
Q

cholesterol synthesis

A

synthesised primarily in the liver, occurs in the cytoplasm and ER. the HMG-CoA reductase reaction is rate-limiting

42
Q

functions of cholesterol

A

cell membranes, sex hormones, hormones released by the adrenal glands, production of bile acids

43
Q

dangers of high cholesterol levels

A

atherosclerosis- increased coronary heart disease risk -> heart attack, angina
-stroke
-peripheral vascular disease

44
Q

statins mechanism of action

A

inhibit an early rate and limiting step in cholesterol biosynthesis, inhibiting hepatic cholesterol synthesis results in increased expression of the LDL receptor gene. Decreased free cholesterol causes membrane-bound regulatory proteins to be cleaved and translocated to the nucleus to bind the sterol responsive element of the LDL receptor gene. This enhances transcription and increases the synthesis of LDL receptors
It also reduces the degradation of LDL receptors

45
Q

what are statins

A

competitive inhibitors of HMG-CoA reductase, decreased cholesterol synthesis, increased expression of the LDL receptor gene.
reduced LDL levels
documented in reducing fatal and nonfatal CHD events, strokes and total mortality

46
Q

statins effects on triglycerides and lipoprotein levels

A

-Decrease triglycerides in hypertriglyceridemic-> 35-45%
-Increase HDL-C
->Normal patients: 5-10%
->Low patients: 15-20%
-Decrease LDL-C ->20-55%
-Non-lipid lowering effects
->Endothelial function (Enhances production of nitric oxide)
->Anti-inflammatory
->Reduce venous thromboembolic events- 43%

47
Q

averse effects of statins

A

Hepatotoxicity
-Elevated hepatic transaminase values
-One case of liver failure per million person-years of use
Myopathy
-One death per million prescriptions caused by rhabdomyolysis

BM213 Pharmacology (4 decks)

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