Medicine - Endocrinology Flashcards

1
Q
Type 1 Diabetes
Pathophysiology:
Symptoms:
Risk factors:
Investigations:
Management:
Complications:
Types of Insulin:
A

Pathophysiology: Absolute insulin deficiency - autoimmune destruction of B cells

Symptoms: Polyuria, Polydipsia, Weight Loss

Risk factors: Genetic inheritance - diagnosed young

Investigations: HbA1c > 6.5% (48mmol/mol), Fasting BG >7mmol/L, Random BG > 11mmol/L, >6.1% = Pre-diabetes

Management: DAFNE, Lifestyle (Carb counting, reduced fat, reduced alcohol, stop smoking), Insulin, Finger Prick x4 daily, 3-6 months HbA1c testing - target 6.5%

Complications: Lipohypertrophy from needle, Insulin Leakage, Hypoglycaemia from insulin
Nephropathy, Neuropathy, Retinopathy, Foot Damage, Raised CVD risk, DKA

Insulin types: Novorapid, Humlin-S, Humulin-I, Glargine, DEGLUDEC

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2
Q
Type 2 Diabetes
Pathophysiology:
Symptoms:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: Tissue resistance to insulin and progressive loss of B cells

Symptoms: Same triad + Persistent infection, visual disturbance, slow healing

Risk factors: Obesity, FH, Ethnicity (Black/Asian), Poor diet, PCOS

Investigations: HbA1c > 6.5% (48mmol/mol), Fasting BG >7mmol/L, Random BG > 11mmol/L, >6.1% = Pre-diabetes

Management: DESMOND, Lifestyle advice (Diet - high fibre, low sugar, Alcohol, Smoking, Exercise), Metformin (initial, always), Gliclazide, Pioglitazone, Exenatide, Sitagliptin

Complications:
Nephropathy (screen using ACR yearly), Neuropathy, Retinopathy, Foot Damage, Raised CVD risk, Immunocompromise

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3
Q
Describe the MOAs of:
Metformin
Sitagliptin
Pioglitazone
Gliclazide
Exenatide
Which should be avoided in CKD?
A

Metformin - reduces insulin resistance

Sitagliptin - DPP4 inhibitor - Raises GLP-1, which inhibits glucagon

Pioglitazone - reduces insulin resistance

Gliclazide - sulfonylurea - increases insulin production

Exenatide - GLP-1 agonist, inhibits Glucagon

Avoid Metformin, Gliclazide and Exenatide/Sitagliptin in CKD

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4
Q

Describe Safe Insulin prescribing (5 marks)

A
  1. Inform patients about how to administer and monitor their insulin levels
  2. Advise patients about hypoglycaemia
  3. Get them to contact DVLA - if hypo happens, must stop driving for 3 months
  4. Sick days - if patient is ill, continue to take insulin
  5. Give the patient an insulin passport
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5
Q
DKA
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: Insulin deficiency -> raised Glucagon and Cortisol -> hyperglycaemia. Less glucose in cells, so lipolysis occurs via B oxidation -> Ketone bodies -> metabolic acidosis -> Fluid loss due to osmotic diuresis

Symptoms: Nausea and Vomiting, Abdominal pain, Confusion

Signs: Hyperventilation, Dehydration signs, Fruity breath

Risk factors: T1DM

Investigations: ABG

Management: IV Saline to >90 systolic, fixed rate Insulin IV, continue long-acting insulin eg. Glargine, Potassium Chloride (hypokalaemia risk), once <14mmol/L glucose, give Glucose 10%, continue until Ketones <0.3mmol/L

Complications: Hypokalaemia, Cerebral Oedema, Pulmonary oedema

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6
Q
HHS
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: Hyperglycaemia without acidosis - slow onset. Caused by increased insulin requirement eg. illness - hyperglycaemia causes osmotic diuresis (dehydration = more hyper)

Symptoms: Confusion, Seizures

Signs: Dehydration signs, Raised BM, not acidotic

Risk factors: T2DM

Investigations: ABG

Management: IV Saline, Vasopressor, IV Insulin, Check Phosphate and Potassium constantly, Potassium Chloride, LMWH

Complications: Stroke/DIC (increased coag), Coma, Seizures, MI

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7
Q
Diabetic Foot Ulcers
Pathophysiology:
Symptoms:
Signs:
Investigations:
Management:
Most common organisms:
Complications:
A

Pathophysiology: Neuropathy and PVD causing damage and loss of healing capability to the foot from diabetes

Symptoms: Loss of sensation, Rocker-Bottom foot (Charcot’s)

Signs: Deep, painless ulcer at a pressure point, with or without Charcot’s

Investigations: Swab and X-ray (check for osteomyelitis)

Management: Tissue Viability Nurse input, Debridement, Swab and give antibiotics, Diabetes management

Common organisms: Staph aureus, E. coli

Complications: Osteomyelitis, Charcot’s (weakening of foot bones due to neuropathy)

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8
Q
Hypoglycaemia
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: < 3.5mmol/L, usually caused by Insulin or Sulfonylureas eg. Gliclazide

Symptoms: Confusion, dizziness, hunger

Signs: Pallor, Clamminess, Low BP (poor peripheral circulation), Tachycardia

Risk factors: Alcoholism, Pregnancy, Eating disorders

Investigations: BMs

Management: Fast-acting carbohydrate x3 20g, then Long-acting carbohydrate, IV Glucagon 1mg (with thiamine for alcoholics to prevent Wernicke’s), IV 20% glucose, normal insulin injection and glucose monitoring

Complications: DVLA must be contacted - cannot drive for 3 months

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9
Q

Describe the effects of these hormones:

Aldosterone
Cortisol
Thyroxine
PTH

A

Aldosterone - Increases Na+, reduces K+, increases H2O, raises BP

Cortisol - Anti-insulin, Increases proteolysis, increases lipolysis, increases gluconeogenesis and glycogenolysis, dampens immune response

Thyroxine - Sympathomimetic -> raises HR, BMR, Breathing rate, causes proteolysis and glycogenolysis and causes brain to develop (cretinism risk)

PTH - Raises Calcium, lowers Phosphate - causes increased calcium uptake from bone/gut and increases Vit D production, affects kidneys

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10
Q
Cushing's Syndrome
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Investigations:
A

Pathophysiology: Raised Cortisol - most commonly due to prescribed glucocorticoids, but can be due to a ACTH adenoma (disease)

Symptoms: Hyperglycaemia with polyuria/polydipsia (steroid diabetes), purple striae, thin arms (proteolysis), central obesity, moon face, buffalo hump (lipolysis), reduced immunity

Signs: Hypertension, Moon face, Buffalo hump, Thin arms, Purple striae

Risk factors: Taking glucocorticoid steroids

Investigations: 9am cortisol level

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11
Q
Addison's disease
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: Adrenal insufficiency - Low Cortisol/low Aldosterone - Autoimmune atrophy of cortex, Stopping steroids, TB (most common cause worldwide)

Symptoms: Muscle weakness, Tiredness, Vague abdominal pain, N+V, Weight loss, Dizziness

Signs: Increased skin pigmentation (POMC -> ACTH and a-MSH), Hypotension, Postural hypotension, Vitiligo

Risk factors: Genetics, stopping steroids, having TB

Investigations: 9am Cortisol test

Management: Hormone replacement - Hydrocortisone and Fludrocortisone (replaces aldosterone)

Complications: Adrenal Crisis, Hypoglycaemia (no longer anti-insulin)

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12
Q
Adrenal Crisis
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: Caused by the sudden stopping of steroids (which is why patients have wristbands/steroid treatment cards - ACTH is suppressed) or by sudden illness

Symptoms: Nausea and vomiting, Confusion

Signs: Hypotension, Dehydration signs, Hypoglycaemia, Hyperkalaemia (Na all pissed out, K kept in)

Risk factors: Steroid use/requirement

Investigations: ABG, Cortisol and Na levels, K levels

Management: Have an IM Hydrocortisone pen at home in case, otherwise IV Hydrocortisone + IV Hartmann’s

Complications: Shock, seizures (hyponatraemia), corrective complications from hyponatraemia

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13
Q
Hyperthyroidism
Pathophysiology:
Symptoms:
Signs:
Investigations:
Management:
Complications:
A

Pathophysiology: Most commonly due to Graves disease - autoimmune permanent activation of TSH receptors

Symptoms: Heat intolerance, Weight loss, Mental/Physical hyperactivity, Diarrhoea, Amenorrhoea, Osteoporosis

Signs: Tachycardia, Shaking/Trembling hands, Lid Lag, Visual Disturbances/Exophthalmos, Pre-Tibial Myxoedema, Dermal changes, AF

Investigations: Thyroxine and TSH levels: T4 high, TSH low

Management: Carbimazole (care, can cause agranulocytosis) + B-blocker for tachycardia

Complications: Thyrotoxicosis, Osteoporosis

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14
Q

Thyrotoxicosis
Symptoms:
Signs:
Management:

A

Symptoms: Diarrhoea, Anxiety, Heat intolerance

Signs: AF, Tremor, Sweating, Palpitations

Management: Carbimazole + B-blockers

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15
Q
Hypothyroidism
Pathophysiology:
Symptoms:
Signs:
Investigations:
Management:
A

Pathophysiology: Hashimoto’s (TSH receptor blocker) is most common, iodine deficiency is most common worldwide

Symptoms: Cold intolerance, Weight gain, Tiredness, Muscle cramps, Cerebellar ataxia (clumsy), Constipation, Menorrhagia

Signs: Bradycardia, Dry Skin, Alopecia, Deep voice, Myxoedema (around eyes)

Investigations: TSH levels and T4 - T4 low, TSH raised

Management: Levothyroxine replacement for life - need to monitor TSH levels every 4 weeks

Complications: Cretinism in infants, neuro retardation in adults

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16
Q
Hypercalcaemia
Pathophysiology:
Symptoms:
Risk factors:
Investigations:
Management:
A

Pathophysiology: Can be primary (parathyroidism), metastasis to spine, myeloma, PTHrP, Thiazides, Sarcoidosis

Symptoms: Stones (calculi), Bones (bone pain), Moans (abdominal pain, constipation), Thrones (polyuria), Psychiatric undertones (confusion, depression)

Risk factors: Thiazides, Sarcoidosis, Myeloma, Hyperparathyroidism

Investigations: PTH test, PET scan, PTHrP test, Vitamin D test

Management: IV Saline, Bisphosphonates eg. Zoledronic Acid and Calcitonin

17
Q
Hypocalcaemia
Pathophysiology:
Symptoms:
Signs:
Investigations:
Management:
Complications:
A

Pathophysiology: Leads to hyperexcitability of the neurones - caused by: Vitamin D deficiency, CKD, Hypoparathyroidism (DiGeorge), Diuretics (Loop), Thyroidectomy

Symptoms: Paraesthesia, Arrhythmias, Tetany, Convulsions

Signs: Paraesthesia, Arrhythmias

Investigations: ECG, PTH, Vitamin D levels, eGFR

Management: Calcium Gluconate IV, Calci-D tablet long term

Complications: Death

18
Q

5 Primary Cancers that metastasise to bone:

A
Breast
Kidney
Liver
Thyroid
Prostate
19
Q
Diabetes Insipidus
Pathophysiology:
Symptoms:
Signs:
Investigations:
Management:
Complications:
A

Pathophysiology: Lack of ADH - either central - hypothalamus damage from brain injury etc., or nephrogenic, whereby kidneys are insensitive to ADH

Symptoms: Large amounts of very dilute urine, increased thirst

Signs: Hypernatraemia

Investigations: ABG

Management: ADH analogues eg. vasopressors

Complications: Dehydration and seizures from hypernatraemia

20
Q
Hypernatraemia
Pathophysiology:
Symptoms:
Signs:
Risk factors:
Management:
Complications:
A

Pathophysiology: Dehydration, Burns, Sweating, Diuresis (eg. Diabetes Insipidus/DKA) - causes brain cell shrinkage, confusion, haemorrhage, neurological damage

Symptoms: Confusion, seizures, brain haemorrhage

Signs: Neurological damage, tachycardia (and other fluid balance signs eg. mucous membranes, skin turgor, weight loss, capillary refill up, radial pulse weak)

Risk factors: Hospital admission

Management: IV Glucose/Saline 5%, Desmopressin IV

Complications: Cerebral oedema, Hyperglycaemia, Brain damage

21
Q
Hyponatraemia
Pathophysiology:
Symptoms:
Management:
Complications (of condition):
Complications (of correction):
A

Pathophysiology: Dilutional, always. Usually too much ADH. Causes: SIADH, PPIs, Thiazides, SSRIs

Symptoms: Usually asymptomatic, but can cause headaches, drowsiness and seizures

Management: Fluid restriction, Furosemide, Lorazepam to stop seizures, Mannitol to protect from cerebral oedema, Hypertonic IV saline

Complications of condition: Seizures due to cerebral oedema

Complications of overcorrection: Central Pontine Demyelination Syndrome and Hyperchlorinaemic Acidosis

22
Q

Hyperkalaemia
Pathophysiology:
Symptoms:
Management:

A

Pathophysiology: Slows down upstroke of depolarisation - rhabdomyolysis, AKI, Addison’s, ACE, Potassium sparing diuretics

Symptoms: Muscle fatigue, Arrhythmias, Asystole

Management: IV Calcium Gluconate, Insulin + Dextrose, Salbutamol, Calcium Resonium