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YEAR 4 - CCC > Primary care - GI & Renal > Flashcards

Primary care - GI & Renal Flashcards

1
Q

What is the pathophysiology of type 1 diabetes?

A

Autoimmune destruction of Beta cells in Islets of Langerhans of pancreas
leading to lack of production of insulin
Glucose cannot be taken up from blood or
converted to glycogen for storage

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2
Q

What is the pathophysiology of type 2 diabetes?

A

Beta cells remain intact but may secrete less insulin
Other cells also become
insensitive to insulin (insulin resistance)

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3
Q

What genes are responsible for type 1 diabetes?

A

HLA-DR3

HLA-DR4

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4
Q

How does type 1 diabetes present?

A

Rapid onset of clinical triad over days/weeks

  • Polyuria
  • Polydipsia
  • Weight loss
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5
Q

What are some long-term complications of diabetes?

A 
Retinopathy
Neuropathy
Nephropathy
Erectile dysfunction
Vascular disease - main cause of death
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6
Q

How does diabetic ketoacidosis present? What would you see on bloods?

A

Nausea + vomiting
Severe confusion
Dehydrated - dry mucus membranes and reduced skin turgor
Ketotic breath
Kaussmal breathing - deep sighing breaths to try breathe off CO2
Generalised GCS

On bloods, would see:

  • high creatinine, sodium, potassium and phosphate
  • low bicarb
  • high glucose
  • low pH
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7
Q

What is the criteria for diagnosis of diabetes?

A

One abnormal plasma glucose in the presence of symptoms

Random blood glucose >11.1mmol/l
Fasting blood glucose >7mmol/l
HbA1c > 47mmol/L

If asymptomatic: 2 fasting venous glucose samples in abnormal range OR OGTT 2hr value >11.1mmol/l

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8
Q

What is the gold standard test for diabetes?

A

Glucose tolerance test

Ask patient to fast overnight, then give 75g of glucose. Check plasma glucose after 2 hrs.
• ≥11.1mmol/L = diabetic
• ≥7.8 and <11.1mmol/L = impaired glucose tolerance
• <7.8mmol/L = non-diabetic

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9
Q

What is the pharmacological management of T2DM?

A

STEP 1 = Metformin 500mg BD after food
If HbA1c >58 16 weeks later add…

STEP 2 = Metformin + sulphonylurea (gliclazide 40mg OD)
If at HbA1c >57 at 6 months consider…

STEP 3 = Insulin, Glitazone, Meglitinides, Incretin mimetics, Acarbose

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10
Q

What class of drug is metformin in?

A

Biguanides

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11
Q

How does metformin work?

A

Reduces rate of gluconeogenesis

Increases insulin sensitivity to increase uptake of glucose by cells but doesn’t affect insulin output

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12
Q

What are some side effects of metformin?

A

GI upset

Weight loss

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13
Q

When is metformin contraindicated?

A

Renal dysfunction

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14
Q

What kind of drug is gliclazide and what does it do?

A

Sulphonylurea
It stimulates pancreatic insulin secretion - can cause hypoglycaemia
Can cause weight gain because insulin is an anabolic hormone

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15
Q

How do glitazones work?

A

Increase insulin secretion and sensitivity to insulin

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16
Q

What are side effects of glitazones?

When are they contraindicated?

A

Fluid-retention - increased risk of HF
Anaemia
Osteoporosis

C/I in cardiovascular disease

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17
Q

What does acarbose do?

A

Decreases breakdown of starch to sugar

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18
Q

What are the side effects of acarbose?

A

Severe flatulence
Abdominal distention
Diarrhoea

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19
Q

Where in the colon is diverticular disease most common?

A

Sigmoid colon

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20
Q

What are the risk factors for diverticular disease?

A 
Low fibre diet
Smoking
Chronic NSAID use
Age
Obesity
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21
Q

How does diverticulitis present?

A 
Altered bowel habit
Abdominal pain - usually left-sided and colicky
Nausea
Flatulence
Symptoms improve on defaecation
Febrile if acute
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22
Q

How does a perforated diverticulum present?

A

Ileus
Peritonitis
Shock

Requires urgent surgical assessment

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23
Q

What is the treatment of diverticulitis?

A

Abx - metronidazole
Fluids
Analgesia - avoid opioids

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24
Q

Difference between Crohn’s and ulcerative colitis: area affected

A

Crohns:

  • any part of GI tract
  • most commonly terminal ileum
  • transmural
  • skip lesions present

UC:

  • colon
  • distal regions worse affected
  • lesions are constant
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25
Q

Difference between Crohn’s and ulcerative colitis: presentation

A

Crohn’s:

  • pain worse after eating
  • normal bowel frequency
  • malnourished due to decreased absorption - vitamin b12 + iron deficiencies
  • mass in right iliac fossa
  • anal fistula/abscess/stricture

UC:

  • diarrhoea with blood + mucus
  • pain worse in morning
  • tenesmus - most commonly affects rectum (proctitis)
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26
Q

What is protective for UC?

A

smoking

appendectomy

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27
Q

What extra-intestinal symptoms are present in IBD?

A

Both:

  • clubbing
  • Pyoderma gangrenosum (but more commonly Crohn’s)
  • Episcleritis
  • Anterior uveitis

Crohn’s:

  • Aphthous ulcers
  • Erythema nodosum (also caused by strep infection, sarcoidosis, sulfonamides, TB)
  • Ankylosing spondylitis

UC:

  • Clubbing
  • Arthropathy
  • Primary sclerosing cholangitis
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28
Q

What is an acute complication of ulcerative colitis?

A

Toxic megacolon = fulminant colitis

  • Acute colonic dilatation so transverse colon is > 6cm diameter
  • Extension of inflammation beyond mucosa
  • Loss of contractility leads to accumulation of gas and fluid
  • Risk of perforation
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29
Q

What investigations are done for IBD?

A
  • Colonoscopy + biopsy
  • MRI to detect fistulae
  • FBC, CRP, B12, folate
  • Faecal calprotectin tests for GI inflammation
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30
Q

Difference between Crohn’s and ulcerative colitis: histopathology

A

Crohn’s:

  • Transmural granulomatous inflammation -> fibrosis + stenosis -> fistulae + abscesses
  • Cobblestone appearance
  • thickened bowel wall

UC:

  • Crypt abscesses = defining lesion
  • Micro ulcers
  • Inflammatory polyps
  • Inflammation is NOT transmural
  • thinned bowel wall
31
Q

What is the treatment for Crohn’s?

A

Smoking cessation

Prednisolone 40mg per day for 1 week then taper by 5mg each week for 7 weeks

Immunosuppressants if recurrent attacks e.g. azathioprine, infliximab

50% require surgery

32
Q

What is the treatment for ulcerative colitis?

A

Steroids to induce remission
5-ASA e.g. mesalazine OD to maintain
Surgery if failing to respond to medical therapy

33
Q

When is mesalazine contraindicated?

A

Aspirin hypersensitivity

34
Q

What drugs does mesalazine interact with?

A

PPIs - they increase the pH so the gastric protection is broken down in the stomach

Lactulose - decreases the pH of stools so it prevents release in the colon

35
Q

What genes are linked to coeliac disease?

A

HLA-DQ2 (95%)

HLA-DQ8

36
Q

What symptoms are most common in coeliac disease?

A

Weight loss
Diarrhoea
Anaemia - iron or b12 deficiency

37
Q

What skin condition is related to coeliac disease?

A

Dermatitis herpetiformis

38
Q

What is seen on histology of coeliac disease?

A

Villous atrophy
Crypt hyperplasia
WBC infiltration

39
Q

How do you diagnose coeliac disease?

A

All tests must be done whilst eating a gluten-containing diet

  1. Total IgA and IgA tissue transglutaminase = 1st choice
  2. If the first test was only weakly positive, test IgA EMA (endomysial antibodies)
  3. If IgA is deficient, test IgG
40
Q

What happens to the liver in chronic liver disease?

A

Liver is replaced by fibrotic tissue and regenerating nodules of hepatocytes

80% of liver parenchyma is destroyed before symptoms arise

41
Q

What are some signs of chronic liver disease?

A
  • Leukonychia
  • Palmar erythema
  • Dupytrens contracture
  • Spider naevi
  • Gynaecomastia
  • Loss of axillary hair
  • Parotid swelling
  • Caput medusa
42
Q

What are some infectious causes of chronic liver disease?

A 
Hepatitis B
Hepatitis C
CMV
Yellow fever
Leptospirosis
43
Q

What drugs can cause chronic liver disease?

A 
Methotrexate
Paracetamol overdose
Amiodarone
Sodium valproate
Nitrofurantoin
Isoniazid
44
Q

What conditions can cause chronic liver disease?

A 
Primary biliary cholangitis
Primary sclerosing cholangitis
Haemochromatosis
Alpha1-antitrypsin deficiency
Wilson's disease (Chr13 - disorder of hepatic copper deposition)
Autoimmune hepatitis
45
Q

What would blood results show in chronic liver failure?

A

Clotting

  • High INR
  • Prolonged PT

FBC
- Thrombocytopenia (low platelets)

LFTs

  • high ALT (a lot more specific)
  • high AST
  • high ALP
  • high bilirubin

U&Es
- high ammonia (the liver converts ammonia to glutamine which can be excreted as urea by the kidneys)

46
Q

Define chronic kidney disease

A

Abnormal kidney structure or function present for >3 months with implications for health

47
Q

What can cause chronic kidney disease?

A

VITAMIN CDE surgical sieve

Vascular - hypertension, renal artery stenosis, heart failure
Inflammatory - glomerulonephritis, pyelonephritis, interstitial nephritis
Autoimmune - SLE
Metabolic - diabetes, renal stones, urinary tract obstruction, hypercalcaemia
Neoplastic - renal cancer
Congenital - renal dysplasia, Alport syndrome, Fabry disease
Environment/endocrine - parathyroid disease, drugs, malnutrition

48
Q

What are the most common causes of chronic kidney disease in the UK?

A
  1. Diabetes mellitus
  2. Glomerulonephritis
  3. Hypertension
49
Q

When does CKD become symptomatic?

A

When eGFR<30 which is stage 4 CKD

50
Q

What are some symptoms of CKD?

A
  • Fluid overload: SOB, oedema, polyuria
  • Anorexia, nausea, vomiting
  • Pruritis
  • Bone pain
  • Insomnia
  • Restless legs
51
Q

What does FBC show in CKD?

A

Normochromic normocytic anaemia i.e. anaemia of chronic disease; due to decreased erythropoietin production

52
Q

What do U&Es show in CKD?

A
  • Low calcium, high phosphate (renal osteodystrophy)
  • Low sodium, high potassium
  • Low bicarb
  • High urea, high creatinine
53
Q

What imaging would you do in CKD? What would you see?

A

Ultrasound scan of kidneys for size, symmetry, anatomy, corticomedullary differentiation and to exlude obstruction

  • Small kidneys (<9cm) except in amyloid, myeloma, diabetes
  • Asymmetrical = renovascular disease
54
Q

What is the gold standard investigation for CKD?

A

Isotopic eGFR

55
Q

What further investigations should you consider for progressive CKD or AKI without recovery?

A

renal biopsy

56
Q

How can you slow renal disease progression?

A
  • Target BP < 140/90; in diabetes target is < 130/80
  • ACE inhibitors
  • Statins
  • Antiplatelets e.g. aspirin
  • Target HbA1C < 53mmol/mol
  • Lifestyle advice: reduce salt intake, smoking cessation, exercise
57
Q

What are some complications of CKD and how can they be managed?

A

Anaemia

  • treat any iron, folate, b12 deficiencies
  • give erythropoietic stimulating agent if Hb<11g/dL

Acidosis - sodium bicarbonate supplements if eGFR < 30

Oedema - high dose loop diuretics (can be combined with thiazide)

Renal osteodystrophy - vitamin D supplements

Restless legs/cramps

  • iron deficiency may be cause
  • sleep hygiene advice
  • gabapentin
58
Q

Which medications are nephrotoxic?

A

A DIAMOND + Li

Aminoglycosides

Diuretics (especially potassium sparing)
Iodine contrasts/immunosuppressants
Antihypertensives e.g. ACEi, ARB
Metformin
Opioids
NSAIDs
Digoxin

Lithium

59
Q

What is the difference in pathophysiology of nephrotic and nephritic syndrome?

A

Nephrotic - increased permeability of podocytes in glomerular capillary membrane to plasma proteins&raquo_space; hypoalbuminaemia

Nephritic - decreased membrane permeability due to inflammatory response

60
Q

What causes nephritic syndrome?

A

Glomerulonephritis from acute post-streptococcal infection

61
Q

How does nephrotic syndrome present?

A

NEPHROTIC

Na+ decreased (hyponatraemia)
Albumin decreased (hypoalbuminaemia) 
Proteinuria
Hyperlipidaemia
Renal vein thrombosis
Orbital oedema
Thromboembolism
Infection (loss of Ig in urine)
Coagulability increase (due to loss of antithrombin II in urine)
62
Q

Due to impaired excretion, what drugs should be avoided/dose reduced in CKD?

A

Digoxin
Aminoglycosides
Acyclovir
Opiates

63
Q

What can cause a relatively low serum creatinine?

A

Low muscle mass:

  • Being elderly due to wasting of muscles
  • Female
  • Amputees
64
Q

What is the diagnostic criteria for DKA?

A

Random glucose > 11
Venous ketones > 3 or urinary ketones 2++
Venous pH < 7.3
Bicarb < 15

65
Q

What is the management of DKA?

A
  1. First bag of fluid over 1 hour (sodium chloride not hartmanns), second bag over 2 hours, third bag over 2 hours and third bag over 4 hours
  2. Fixed rate insulin 0.1units/kg/hour
  3. Monitor potassium because at risk of hypokalaemia (insulin drives potassium into the cells)
66
Q

What is the DKA equivalent for type 2 diabetes?

A

HHS = hyperosmotic hyperglycaemia state

67
Q

What often precipitates HHS?

A

Underlying infection

68
Q

How do you diagnose HHS?

A
  • Hypovolaemia
  • Hyperglycaemia > 30 mmol/L
  • Without significant hyperketonaemia
  • Without significant acidosis
  • Osmolality > 320mosmol/kg (glucose + urea + 2xNa)
69
Q

What is the management of HHS?

A

Mainstay treatment = fluid resuscitation
Consider IV insulin (half as much as in DKA so 0.05units/kg/hr
Prophylactic LMWH

70
Q

What are the benefits of metformin?

A
  1. Protects the heart
  2. Weight neutral
  3. Doesn’t cause hypos
71
Q

What injectable, other than insulin, can be used in type 2 DM?

A

GLP-1 agonist

  • Reserved for particularly overweight people
  • Delays gastric emptying
  • Once daily injection
  • Must prove 11mmol HbA1c reduction in 6 months
72
Q

What diabetes drug reduces glucose reabsorption in kidney?

A

SGLT-2 inhibitors - cause you to wee out more glucose

73
Q

What are the side effects of SGLT-2 inhibitors?

A

UTIs
Thrush
Weight loss
Slight increased risk of DKA with canagliflozin

YEAR 4 - CCC (7 decks)

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