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1
Q

What is the role of the kidneys?

A

Filtration
Tubular reabsorption
Tubular secretion

Regulation
Endocrine

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2
Q

How does the kidney handle electrolytes?

A

Sodium - reabsorbed in PCT and fine tuned in loop of henle

Potassium - reabsorbed in PCT but secreted in distal tubule under aldosterone control

Calcium and phosphate - regulated by parathyroid hormone and vitamin D

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3
Q

What happens if GFR decreases?

A

Decrease of urea in urine
Increased urea in blood
Decreased potassium in urine

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4
Q

What is glomerulosclerosis?

A

Thickening of the lumen can be cause my hypertension and diabetes.

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5
Q

What is AKI?

A

A rapid loss of renal function with signs of reduced urine output, oedema, hypertension, N+V and confusion. It is diagnosed on serum creatinine and urine output.

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6
Q

What are the causes of AKI?

A

Prerenal means a reduced perfusion and can be caused by volume depletion, drugs etc.

Intrinsic is due to pathological damage to the kidney such as glomeruloneohritis, nephrotoxicity etc.

Postrenal is an obstruction to urine flow back which inhibits filtration.

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7
Q

What are complications of AKI?

A

Fluid overload
Metabolic acidosis due to decreases H+ secretion
Hyperkalaemia due to impaired potassium homeostasis.

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8
Q

How do we manage AKI?

A

Eliminate stressor
Fluid resuscitation for dehydration
Loop diuretics for oedema or GTN. Restrict salt and fluid intake.
Sodium bicarbonate for metabolic acidosis (cautioned in hyperkalaemia)

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9
Q

What do we do in cases of hyperkalaemia?

A

1.protect heart using calcium gluconate to stabilise cardiac rhythm

2.redirect potassium into cells using insulin for salbutamol. Both stimulate Na+/K+ ATPase pump.

3.remove potassium from body using sodium zirconium. This is lokelma.

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10
Q

What is CKD?

A

Progressive irreversible loss of nephrons due to disease or ageing.

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11
Q

How do we assess CKD?

A
  1. Assess severity and course
  2. Determine kidney function
  3. Determine dosing regime
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12
Q

What are the markers for CKD?

A

Proteinuria and haematuria due to altered glomerula integrity

Decreased excretion

Decreased hormonal synthesis causes anaemia and hypocalcaemia

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13
Q

How do we manage CKD?

A

Manage causation
Use ACE inhibitors to protect kidney, suppress RAAS, reduce glomerular pressure etc.
Can also use SGLT-2 inhibitors to inhibit renal glucose reabsorption.

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14
Q

What are loop diuretics?

A

Block Na+/K+/2Cl- symporter

Can be used in AKI to improve diuresis

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15
Q

What are side effects of loop diuretics?

A

Hypokalaemia
Decreased reaborption of calcium and magnesium

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16
Q

What are thiazide like diuretics?

A

Block symporter in early DCT

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17
Q

What are SE of thiazide like diuretics?

A

Hypokalaemia
Metabolic alkalosis
Dehydration
Hypotension
Hyponatremia

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18
Q

What is nephrotoxicity?

A

Rapid deterioration in kidney function as a result of medications and chemicals.

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19
Q

What are drug factors in nephrotoxicity?

A

Prolonged exposure
Combinations
Insoluble drug causing intratubular crystal precipitation

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20
Q

What are kidney factors in nephrotoxicity?

A

High blood delivery
Increased conc
Bioteabsformations

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21
Q

What are patient factors in nephrotoxicity?

A

Female
Old age
Cirrhosis
Disease
Pharmacogenetics

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22
Q

What are signs and symptoms of nephrotoxicity?

A

Decreased GFR
Increase blood urea
Decreased urine
Increased creatinine
Electrolyte imbalance
Fluid retention

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23
Q

What is viral hepatitis?

A

Inflammation of the liver tissue caused by infections A-E.

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24
Q

Is hep A chronic or acute?

A

Acute

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25
How is hep A transmitted?
Orofecal
26
How is hep A treated?
No antiviral drug available to treatment is supported. Vaccine available
27
How is Hep B transmitted?
Perinatally Sexually
28
What is Hep B risk?
People from endemic regions IV drug users Multiple sex partners Immunocompromised
29
How is hep C transmitted?
Mainly parentally through blood Sexual transmission is rare
30
What is the role of the liver?
Energy metabolism Bile production Detoxification and clearance!!
31
What is the livers dual blood supply?
Hepatic artery and portal vein
32
How does the liver work in energy metabolism?
The liver metabolises carbohydrates, fatty acids, amino acids and proteins. It is also the main site for cholesterol metabolism.
33
How is the liver an excretory organ?
Ammonia from amino acids is converted into urea and secreted into the blood It removes unconjugated bilirubin Synthesises bile acids from cholesterol Inactivates many enzymes from endocrine cells
34
What is liver disease?
A build up of scar tissue formed when the liver is damaged. This causes nodules that replace the usually smooth tissue changing the shape and workings of the liver
35
What is cirrhosis?
Develops as a result of progressive damage to the liver over a number of years. It can be compensated or decompensated.
36
What is the prognosis of cirrhosis determined by?
Underlying cause Lifestyle changes Complications
37
What is portal hypertension?
Increased pressure in the portal vein due to chronic end stage liver disease, leading to hepatic vascular resistance. The blood goes anywhere it can and backs up.
38
What is hepatic encephalopathy?
The liver cannot detoxify ammonia from the blood. The build up of nitrogen compounds enters the BBB and causes altered behaviour.
39
What is WE?
Wernickes is caused by a lack of thiamine usually in alcoholics
40
What is ascites?
Accumulation of fluid in the peritoneal cavity due to vasodilation and retention.
41
What are varices?
Dilated blood cells due to regular blood flow being blocked. Can haemorrhage.
42
What is DILI?
Drug induced liver injury is a rare side effect of some medicines causing tiredness, loss of appetite, jaundice, itching etc.
43
How is PK affected in liver disease?
A - changes in bioavailability if the drug is subject to first pass metabolism D - may be affected due to a reduction in plasma binding proteins M - decrease in CYP enzymes E - change in hepatic clearance.
44
Why do people get jaundice?
Increase in bilirubin as it is not broken down in cirrhosis. Can also cause itching
45
Why do people get coagulopathy?
Prolonged clotting time and low platelets.
46
Why do people have a higher risk of SBP?
Bacterial infection of the abdomen caused by ascites
47
How do we acutely manage alcohol withdrawal?
CIWA-Ar protocol depending on symptoms If >11 give diazepam 20mg PRN
48
How do we acutely treat encephalopathy?
Pabrinex
49
How do we prophylactically treat WE?
Thiamine depending on severity
50
How do we phrophylacticallg treat HE?
Lactulose with an aim of 2-3 loose stools a day. Reduces amount of time for ammonia to be absorbed by reducing transit time Rifazamin 550mg BD to reduce production and absorption of ammonia
51
How do we treat PVH?
Propanolol 40mg BD increased to 160mg BD if necessary. Carvedilol is unlicensed but started at 6.25mg daily and increased as needed
52
What are CI of beta blockers?
Bradycardia Asthma Bypotension
53
What do we give for coagulopathy?
Vitamin K 10mg OD STAT max 5 days
54
Why must we give vitamin K slowly
Anaphylaxis in IV admin
55
How do we treat ascites?
Spironolactone 100-400mg OD
56
What is CI for spironolactone?
Hyperkalaemia and Addisons disease
57
What drug can we give for varices?
Terlipressin IV
58
How do we treat non alcoholic fatty liver disease
Pioglitazone Vitamin E in advanced fibrosis
59
When is pioglitazone CI?
Heart failure Bladder cancer
60
When is pioglitazone CI?
Heart failure Bladder cancer
61
What is haemochromatosis?
Excessive iron absorption Genetic
62
What is AAT deficiency?
Causes an increase in the breakdown of elastin by the reduced inactivation of elastase. Responds well to asthma treatment
63
What is Wilson disease?
Copper accumulation as the liver can’t process. Can lead to neurological disorders and liver failure

Liver and Kidney (1 decks)

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