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PMP202 > Kidney + liver > Flashcards

Kidney + liver Flashcards

1
Q

define nephrotoxicity

A

rapid deterioration in kidney function as a result of medications and chemicals

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2
Q

List types of nephrotoxic drugs and intoxicants

A
  • prescribed drugs
    -OTC
    -herbal remedies
    -Food products
    -recreational drugs
    -imaging agents
    -moulds + fungi
    -cancer therapeutics
    -antibiotics
    -some metals e.g. lead and mercury

e.g. Vancomycin, Mitomycin, NSAIDs, ACEi, ARBs, radiocontrast

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3
Q

Explain why not all nephrotoxic drugs affect patients equally

A
  • some patients are more susceptible due to genetics
    -patients have different metabolism and excretion of compounds
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4
Q

Discuss how drug characteristic e.g. solubility, structure, and charge can effect nephrotoxicity

A

solubility - may cause acute crystalline ppt in DCT if insoluble in urine + made worse by reduced urinary flow rates + excessive drug dosing e.g. methotrexate
structure - need to slowly rehydrate individuals because cell swelling can occur with drugs such as dextran.
charge - drugs with positive charge e.g. polycationic aminoglycosides are attracted to negatively charge PCT membrane phospholipids which facilitates drug binding to receptor complexes.

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5
Q

Explain how patient characteristics can effect whether a drug is nephrotoxic to them

A
  • what their blood volume is
  • electrolyte imbalance
  • infection
  • age, ethnicity, sex
  • co-morbidities
    -dehydration
    -AKI + CKD
    -nephrotic syndrome
    -genetics + mutations
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6
Q

Explain how kidney structure and function determines nephrotoxicity

A

volume repletion
loading doses
phase 1 reactive oxygen species
ischemia of cells
transporters for uptake of drugs

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7
Q

Explain the aetiology of common causes of impaired kidney function including polycystic Kidney disease

A
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8
Q

what are the causes of AKI

A
  • prerenal - impairment of blood supply to kidneys from volume depletion or drugs such as NSAIDs
  • intrinsic - impairment within kidney’s blood vessels, glomeruli + tubules can happen from immune response, damage due to antibiotics or heavy metals or infection
    -postrenal - obstruction of the urinary collecting system e.g. swelling of blood vessels leading to ischaemia or obstruction such as kidney stones.
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9
Q

what are risk factors of AKI

A
  • poor fluid intake
  • dehydration
    -drugs
    -infection
    -trauma
    -rhabdomyolysis
    -volume depletion
    -hypotension
    -low cardiac output
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10
Q

what is the pathophysiology of AKI

A

sudden decrease in kidney function due to reduced urine output, urine retention or fluid overload.

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11
Q

what are the complications and management of AKI

A

diagnosis based on serum creatinine or urine output

fluid overload e.g. oedema - loop diuretics e.g. furosemide

dehydration - fluid resuscitation

metabolic acidosis - sodium biocarbonate

Hyperkalaemia (emergency) - when >7mmol/L more prominent T wave use of calcium gluconate to antagonise the membrane excitability, redirect K+ from blood to cells using insulin + glucose, salbutamol, sodium biocarbonate, haemodialysis.

Find the underlying cause

if infection - antibiotics
if obstruction - remove or empty bladder
if toxic drugs - stop taking.

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12
Q

describe the causes and risk factors of chronic kidney disease

A

-disease
-injury
-ageing
-hypertension
-hyperglycaemia
-hyperlipidaemia
-renal infections
-post-renal obstruction
-drugs e.g. NSAIDs

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13
Q

what is the pathophysiology of chronic kidney disease?

A

progressive, irreversible loss of nephrons due to disease, injury or ageing.

early - primary insult –> nephron number decreases –> increase in glomerular pressure –> vasodilation of surviving nephrons–> homeostasis–> keeps happening causes glomerular sclerosis

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14
Q

what are the complications and management of chronic kidney disease?

A
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15
Q

what is the mechanism of action for chelating agents used for kidneys?

A

Forms a chelate complex with a metal ion forming a strong stable ring structure when binding with a polydentate. Kf/formation constant helps to determine the stability.

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16
Q

what is the mechanism of action of phosphate binding agents used for the kidneys?

A

phosphate binding agents - form insoluble compounds in the GI tract so they cannot be absorbed into the body, so they are excreted out. e.g. Calcium acetate, calcium carbonate, aluminium salts

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17
Q

what is the mechanism of action of thiazide diuretics used for the kidneys?

A

promotes diuresis, blocks Na/Cl transporter –> inhibits reabsorption of Na and Cl ions –> increases elimination of water from the body

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18
Q

what is the MOA of calcimetic agents

A

mimic action of calcium on tissues, binds at allosteric site acts on calcium sensing receptors e.g. Cinacalcet

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19
Q

what does alfacalcidol do?

A

promote calcium homeostasis and bone metabolism

an analogue of vit D3 (Vit D3 gets hydroxylated at C25, then further at 24 or 1 alpha. Those with renal failure cannot perform alpha 1 hydroxylation so are given alfacalcidol

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20
Q

advantages of sustained/controlled release

A
  • reduces the dose frequency
    -minimal fluctuations for desired therapeutic effect
    -reduced side effects
    -reduce total drug
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21
Q

discuss the different types of modified drug release

A

delayed release - drug released some time after administration (enteric coated+pulsatile)

extended release - prolonged release to reduce dose freq(sustained + controlled)

targeted release - inc conc of medication in some parts of the body (passive + active targeting)

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22
Q

key points of controlled drug release

A

delayed - enteric coated protects from gastric acid or patient from irritation. Pulsatile released based on repeated succession of pulses at time intervals.

extended sustained - maintains rate of drug release over sustained period but not at a constant rate - prolong time in therapeutic range. Only oral

extended controlled - drug released at nearly constant rate + Cp independent of biological environment. Variety of dosage forms e.g. transdermal systems.

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23
Q

How do the two types of diffusion controlled release mechanisms work?

A

Matrixes - Monolithic where drug molecules diffuse through pores or between chains.

Reservoirs - drug released from an insoluble polymeric semi - permeable membrane that encapsulates the drug e.g. a transdermal patch (membrane controlled).

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24
Q

How does osmotic drug delivery mechanism work?

A

polymer - controlled release agent swells and releases the drug. Usually from absorbing water or bodily fluids

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25
Q

How does dissolution/degradation mechanism of drug delivery work?

A

Biodegradable polymers
degrade by natural processes either the surface erodes or the bulk.

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26
Q

How does responsive controlled drug release mechanism work?

A

responds to a stimuli e.g. pH or electrical current that allow for the drug to be released

27
Q

describe the various gastroretention systems

A
28
Q

advantages and disadvantages of targeted drug delivery

A
29
Q

how are drugs cleared from the kidneys and liver

A
30
Q

how are drugs targeted to be delivered to the kidneys and liver

A
31
Q

provide examples for site-specific drug delivery systems

A
32
Q
A
33
Q

what are the transmission routes of hepatitis B and C?

A

Blood, sexual or vertical (mother)

34
Q

outline the pathogenesis hepatitis B

A
  • asymptomatic - incubation period 4-12 weeks replicates in hepatocytes without symptoms
  • acute phase - HBV detected in plasma –> T -cell response causes hepatocellular necrotic damage. Early response - cytokines released no cytolytic effect. Late response causes liver damage and inflammation. Can resolve on its own within 6 months.
35
Q

Pathophysiology of hepatitis B

A

After chronic phase (6 months)
- CD8 T cell response fails and liver necrosis and inflammation occurs.
-causes cirrhosis of the liver and leads to permanent scaring –> hepatocellular carcinoma
-HBV is an oncovirus so can lead to cancer transformation –> hepatocellular carcinoma

36
Q

what are the clinical manifestations of hepatitis B?

A

-pre-icteric phase : fever, nausea, serum alt levels rise
-icteric phase: (3-10 days) jaundice, systemic symptoms, enlarged liver
-resolution phase: icteric symptoms resolve + fatigue may last

37
Q

How do you manage and treat hepatitis B?

A

target the reverse transcriptase using anti-HBV drugs

resemble natural nucleosides and terminate viral DNA by incorporation into the viral DNA.

e.g. Lamivudine, Entecavir, Telbivudine

Use of Peg-IFNalpha - 2a - pegylated derivatives of interferon alpha help to boost the immune system.

patients should be monitored every 6 months for viral load and renal function.

desired outcome HBV undetectable levels to prevent disease progression. Treatment usually lifelong

38
Q

How do you manage and treat hepatitis C?

A

Harvoni OD - HCV polymerase inhibitor
Zepatier OD - HCV protease inhibitor
Epclusa OD - HCV polymerase inhibitor
Mavret TDS - HCV protease inhibitor

39
Q

what is the location and structure of components on the urinary system?

A

consists of: inferior vena cava, adrenal gland, aorta, renal artery, renal hilum, renal vein, kidney, ureter, lilac crest, uterus, urinary bladder, urethra

40
Q

what are the structure, blood supply, nerve supply and function of the kidney?

A

functions of kidneys:
- regulate blood volume
-removal of urea from bloodstream
-conserve nutrients
-regulate acid-base balance
-regulate blood pressure
-calcium homeostasis
-production of erythropoeitin and renin

Blood and nerve supply:
Aorta –> renal artery–>segmental artery–>interlobular artery –> arcuate artery –> cortical radiate artery –> Afferent arteriole –> glomerulus –> efferent arteriole–> peritubular capillaries –> cortical radiate vein –> arcuate vein –> interlobular vein –> renal vein –> inferior vena cava

41
Q

describe regulation of micturition

A

urinary bladder stretches –> afferent impulses from stretch receptors to simple spinal reflex or brain.
Promotion of micturition when: increased parasympathetic activity, decreased sympathetic activity, decreased somatic motor nerve activity –> Detrusor muscle contracts, internal + external sphincter open

Inhibition of micturition when: Goes to brain, pontine storage centre, acts on three spinal efferents –> decreased parasympathetic activity, increased sympathetic activity, increased motor nerve activity

42
Q

explain the anatomy of a nephron in relation to the formation of urine

A

glomerulus –> bowman’s capusle (glomerular filtration) –> PCT (tubular reabsorption + secretion) –> loop of henle –> DCT –> collecting tubule –> collecting ducts –> calyces –> renal pelvis –> ureter –> urinary bladder –> urethra.

43
Q

explain the 3 processes of urine formation

A

Filtration (blood to nephron tubules)
Tubular reabsorption - passive and active returning material to blood from filtrate e.g. glucose, Na+, HCO3-
Tubular secretion - removing material from blood to filtrate e.g. urea

44
Q

describe the regulation of water, acid, base and electrolyte balance in the kidney

A

water - controlled by ADH released by posterior pituitary in response to low blood volume or high osmolarity (Na).
acid + base - HCO3- combines with H+ to form H2CO3, carbonic anhydrase converts H2CO3 into H2O and CO2. This regulates urine and blood pH
electrolyte - symporters and transporters help to move electrolytes such as Na.

45
Q

liver disease symptoms

A

Early stages/compensated:
- bruising
-fatigue
-abdominal pain
-loss of appetite
- weightless + muscle wasting
- dark urine
- N + V
-spider navi
-disturbed sleeping patterns

decompensated:
- jaundice
- ascites - build up of fluid in abdomen
-coagulopathy - bleeding risks
-increased infections
-encephalopathy - confusion
-increased sensitivity to drugs + alcohol

46
Q

symptoms of liver cirrhosis - liver failure

A
  • Jaundice (increased bilirubin causes yellow colour) can cause itchiness and pale stools
  • Encephalopathy:
    Wernicke’s - caused by thiamine deficiency
    Hepatic - caused by build up of toxins in the blood e.g. nitrogen compounds increases permeability of BBB.
    can cause sleep disturbances, motor problems, behavioural changes

-Coagulopathy:
prolonged clotting times, low PLT, prolonged prothrombin time

47
Q

symptoms of cirrhosis - portal vein hypertension

A
  • Ascites: portal vein clot + increased resistance in blood flow due to scarring and pushes fluid into abdominal space causing bloating and pain. Na and water retention and splanchnic vasodilation.

-Spontaneous bacterial peritonitis: Bacterial infection in patient abdomen due to ascites causes fever, increased HR, chills

-variceal haemorrhage: dilated veins in oesophagus + abdomen bodies way of reducing BP in hepatic portal vein. contributes to encephalopathy as blood by-passes the liver and can lead to bust haemorrhage. Blood in vomit + stool.

-portal vein thrombus:

48
Q

how do you treat acute alcohol withdrawal

A

-Use NICE the CIWA-Ar protocol (based on symptoms, score >11 suggests severe and assessed every 1-2 hours.
- Diazepam 20mg PRN (PO) when CIWA-Ar >11 (benzodiazepine)
- Diazepam 10mg PRN (PR) if the patient has a seizure
- Adrenaline 1:1000 (IM) if patient has anaphylactic reaction to pabrinex.

49
Q

How do you treat + manage encephalopathy?

A

Wernicke’s (vit B deficiency):
Acute management
Pabrinex (IV or IM) 2 pairs TDS 5 days, then 1 pair OD (make sure patient isn’t on any thiamine whilst using)
Prophylaxis:
Thiamine (PO):
Mild - 50mg-100mg daily
severe - 200mg - 300mg daily (divided doses for both)

Hepatic (build up of nitrogen compounds):
prophylaxis:
Lactulose 30-50ml TDS aim for 2-3 stools per day (less time for ammonia to be reabsorbed into the circulation)
Rifaxamin 550mg BD (reduces production and ammonia reabsorption) used alongside lactulose.

50
Q

How do you treat portal vein hypertension

A

reduces ascites, abdominal varices and portal vein thrombi
- Propranolol - 40mg BD (max 160mg BD)

-Carvedilol (unlicensed indication) - 6.25mg daily

51
Q

How do you treat coagulopathy?

A

vitamin K OD (PO or IV) 10mg stat for max 5 days + monitor prothrombin time and signs of bleeding

hold anticoagulants

52
Q

How do you treat ascites?

A

managed with diuretics to remove fluid build-up or drain in severe cases

Spironolactone 100mg-400mg OD
monitor Cr + K+ + weight

53
Q

How do you treat spontaneous bacterial peritonitis (SBP)?

A

No pen allergy:
Tazocin (IV) 4.5g TDS

non - severe pen allergy:
Cefotaxime (IV) 2g TDS
Metronidazole (IV) 500mg TDS

severe pen allergy:
Co-trimoxazole (IV) 960mg BD
Metronidazole (IV) 500mg TDS
Gentamycin (IV) 5mg/kg OD

Prophylaxis:
1st line: co-trimoxazole (PO) 960mg OD
2nd line: Ciprofloxacin (PO) 500mg OD

54
Q

How do you treat oesophageal + abdominal varices?

A

endoscopic intervention e.g. variceal band ligation (prevents bleeding)

If rupture does occur:
Terlipressin (IV) 1mg -2mg QDS max 72 hrs (vasopressin analogue –> vasoconstriction)
kept in the fridge

55
Q

medications to avoid in Werneck’s encephalopathy (vit B deficiency)

A

medications that cause constipation e.g. opioids + slow gut motility

56
Q

medications to avoid in hepatic encephalopathy (nitrogen build up to brain)

A

medications that sedate e.g. analgesics, opioids, gabapentiniods, antipsychotics, sedatives, benzos, sleeping tablets

57
Q

medications to avoid in coagulopathy/varices

A

anticoagulants + antiplatelet treatment e.g. NSAIDs, aspirin

58
Q

medications to avoid due to ascites (fluid overload)

A

drugs that cause fluid retention e.g. steroids, NSAIDs, CCBs

59
Q

medications to avoid due to lowered drug metabolism

A

drugs that are metabolised by the liver or secreted in bile unchanged.

60
Q

medications to avoid due to decreased protein synthesis

A

drugs with high protein - binding potential = increased risk of toxicity e.g. phenytoin, prednisolone

61
Q

medications to avoid due to hepatotoxicity

A

Methotrexate, sodium valproate, amiodarone etc.

Patient finds dose toxic at lower doses

62
Q

risk factors for NAFLD

A

obesity, impaired glucose reg, T2 diabetes, hypertension, hyperlipidaemia, FHx, endocrine disorders, drugs, other liver conditions, obstructive sleep apnoea

63
Q

what complications can occur in NAFLD

A
  • same as alcoholic liver disease
  • increased risk of HTN, CKD, type 2 diabetes, impaired glucose regulation, CVD
64
Q
A

PMP202 (5 decks)

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