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Phase 2a Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define DIABETES MELLITUS

A
  • Chronic hyperglycemia due to insulin dysfunction
  • can’t move glucose from blood into cells
  • low glucose in cells so they starve of energy
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2
Q

epidemiology of TYPE 1 DIABETES MELLITUS

A
  • early onset <30 yrs old
  • usually lean
  • northern european ancestry
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3
Q

epidemiology of TYPE 2DIABETES MELLITUS

A
  • older onset >30 yrs
  • overweight
  • common in african/asian people
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4
Q

list 8 risk factors for TYPE 2 DIABETES MELLITUS

A

Modifiable

1) . obese
2) . hypertension
3) . hyperlipidemia
4) . drinking excess alcohol
5) . sedentary lifestyle

Non-modifiable

1) . older
2) . family history
3) . asian/african heritage

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5
Q

list 3 causes of TYPE 1 DIABETES MELLITUS

A
  • HLA DR3/4 (cell surface receptors) affected in >90% of people
  • autoimmune disease which targets islet cells
  • family history
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6
Q

list 5 potential cause of TYPE 2 DIABETES MELLITUS

A
  • pancreatic (pancretitis, surgery, trauma, destruction, cancer)
  • cushing’s disease
  • acromegaly
  • hyperthyroidism
  • pregnancy
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7
Q

outline the general pathology of TYPE 1 DIABETES MELLITUS

A
  • Autoimmune destruction of pancreatic B-cells in Islets of Langerhans
  • Associated with HLA genetics
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8
Q

explain the pathology of polyuria in TYPE 1 DIABETES MELLITUS

A
  • blood glucose exceeds the renal tubular reabsorptive capacity
  • leads to osmotic diuresis (increased urination rate)
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9
Q

explain the pathology of weight loss in TYPE 1 DIABETES MELLITUS

A
  • fluids have been depleted + insulin deficiency

- leads to muscle and fat breakdown

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10
Q

briefly outline the pathology of TYPE 2 DIABETES MELLITUS

A
  • B-cell mass reduced to 50% of normal
  • low insulin secretion + peripheral insulin resistance
  • beta cell hypertrophy + hyperplasia to create more insulin to remove glucose from blood
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11
Q

what is the length of history you assess for in TYPE 1 DIABETES MELLITUS

A

2-6 weeks

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12
Q

list 4 signs / symptoms for TYPE 1 DIABETES MELLITUS

A
  • polydipsia (excessive thirst)
  • polyuria (excessive urination)
  • weight loss
  • polyphagia (excess appetite)
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13
Q

if TYPE 1 DIABETES MELLITUS is not picked up fast, what is another symptom and what does it indicate

A
  • fruity breath -> indicates KETOACIDOSIS
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14
Q

explain the pathology of polydipsia in TYPE 1 DIABETES MELLITUS

A
  • excessive thirst

- due to fluid / electrolyte loss

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15
Q

list 4 signs/symptoms for TYPE 2 DIABETES MELLITUS

A

usually >asymptomatic< BUT…

  • Central obesity
  • elevated cholesterol
  • elevated triglycerides
  • raised BP
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16
Q

list 2 investigations for TYPE 1 DIABETES MELLITUS

A
  • Fasting plasma glucose

- random plasma glucose

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17
Q

what should be the results of the FASTING plasma glucose in TYPE 1 DIABETES MELLITUS

A

> 7.0 mmol/L

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18
Q

what should be the results of the RANDOM plasma glucose in TYPE 1 DIABETES MELLITUS

A

> 11.1 mmol/L

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19
Q

what is required for a diagnosis of TYPE 1 DIABETES MELLITUS

A

Symptoms of hyperglycemia + 1 or more of:

  • ketosis
  • rapid weight loss
  • age of onset <5 yrs old
  • BMI < 25KG/M²
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20
Q

outline the management of TYPE 1 DIABETES MELLITUS

A
  • insulin twice daily with meals

- glycaemic control via diet -> low sugar/fat foods

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21
Q

list 4 investigations for TYPE 2 DIABETES MELLITUS

A
  • HbA1C
  • random blood glucose
    fasting blood glucose
  • oral glucose tolerance test (GTT) 2 hrs post meal
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22
Q

briefly describe the HbA1C test

A
  • tests proportion of Hb in RBC that has a glucose on it (glycated haemoglobin)
  • gives indication of how long blood glucose levels have been high
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23
Q

expected result for FASTING plasma glucose in suspected TYPE 2 DIABETES MELLITUS

A

> 7mmol/L

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24
Q

expected result for RANDOM plasma glucose in suspected TYPE 2 DIABETES MELLITUS

A

> 11.1mmol/L

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25
Q

expected result for oral GTT 2 hrs post meal in suspected TYPE 2 DIABETES MELLITUS

A

> 11.1mmol/L

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26
Q

expected result for HbA1c in suspected TYPE 2 DIABETES MELLITUS

A

> 47mmol/L

>6.4%

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27
Q

list 4 scenarious where you wouldn’t use HbA1c

A
  • pregnancy
  • children
  • T1DM
  • pancreatic surgery
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28
Q

list 3 diagnostic criteria combinations for TYPE 2 DIABETES MELLITUS

A

1) symptoms of hyperglycemia + 1 abnormal glucose result
2) asymptomatic + 2 separate abnormal glucose results
3) abnormal HbA1c

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29
Q

outline 4 non-pharmacological management of TYPE 2 DIABETES MELLITUS (try these before giving drugs)

A
  • diet excercise changes
  • patient education
  • smoking cessation
  • regular blood glucose monitoring using HbA1c
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30
Q

outline the pharmacological treatment pathway for TYPE 2 DIABETES MELLITUS

A

1st line)
- Biguanide (METFORMIN)

2nd line)

  • metformin AND*
  • sulphonylurea
  • DPP4 inhibitor
  • pioglitazone

3rd line)
- insulin

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31
Q

Drug class - BIGUANIDE. Give an example.

A

METFORMIN

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32
Q

Drug class - BIGUANIDE. Give mechanism of action

A
  • reduce gluconeogenesis in liver (this is increased in T2DM bc of excess glucagon)
  • increased uptake/utilisation of glucose in skeletal muscle (increased insulin sensitivity)
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33
Q

Drug class - BIGUANIDE. give contraindications

A
  • people with renal (main one) / liver problems
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34
Q

Drug class - BIGUANIDE. give side effects

A

1) . GI disturbance (leads to weight loss!!)
- abdo pain
- anorexia
- diarrhoea
- nausea

2) . lactic acidosis (rare) in:
- renal disease
- liver disease

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35
Q

Drug class - SULPHONYLUREA. give 2 examples

A
  • gliclazide

- glipizide

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36
Q

Drug class - SULPHONYLUREA. give mechanism of action

A
  • stimulate B cells to secrete more insulin
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37
Q

Drug class - SULPHONYLUREA. give contraindications

A
  • pregnancy / breastfeeding -> can cross the placenta and enter breast milk
  • may cause hypoglycemia in newborns
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38
Q

Drug class - SULPHONYLUREA. give side effects

A
  • hypoglycemia

- weight gain (stimulates appetite)

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39
Q

Drug class - DPP4 INHIBITORS. give example

A

Stigaliptin

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40
Q

Drug class - DPP4 INHIBITORS. Give mechanism of action

A
  • inhibit DPP4 -> stopping breakdown of incretins GLP-1/GIP
  • GLP-1/GIP stimulate insulin secretion

DPP4 normally inhibits incretins

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41
Q

Drug class - THIAZOLIDINEDIONES. give example

A

proglitazone

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42
Q

Drug class - THIAZOLIDINEDIONES. give mechanism of action

A
  • enhance fatty acid / glucose uptake -> body makes more fat from these
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43
Q

Drug class - THIAZOLIDINEDIONES. give side effects

A
  • fluid retention

- weight gain

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44
Q

what might you also give DIABETICS so they have cardiovascular protection?

A
  • statins

- antihypertensives

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45
Q

list 7 DIABETIC complications

A

1) diabetic nephropathy
2) diabetic neuropathy (lack of foot sensation -> ulcers etc)
3) diabetic retinopathy (blood shot eyes -> sight loss)
4) erectile dysfunction
5) arterial disease (IHD / MI)
6) Staph skin infections
7) Diabetic ketoacidosis

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46
Q

HYPOGLYCAEMIA - aetiology

A

insufficient glucose to brain

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47
Q

HYPOGLYCAEMIA - cause

A

complication of insulin of sulfonylurea therapy

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48
Q

HYPOGLYCAEMIA - whats the blood glucose threshold

A

below 3mmol/L

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49
Q

HYPOGLYCAEMIA - list 5 signs and symptoms

A

1) . odd behaviour (aggression)
2) . sweating
3) . tachycardia (fast HR)
4) . hunger
5) . pallor (unhealthily pale)

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50
Q

HYPOGLYCAEMIA - how would you diagnose

A

blood glucose level test

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51
Q

HYPOGLYCAEMIA - 2 ways you would manage

A
  • glucose (IV/Food)

- glucagon

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52
Q

DIABETIC KETOACIDOSIS - what is it

A
  • state of uncontrolled hyperglycemia and catabolism (breakdown)
  • associated with insulin deficiency
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53
Q

DIABETIC KETOACIDOSIS - outline the general pathophysiology

A

1) . no insulin so LOTS of hepatic gluconeogensis
2) . lots of glucose -> osmotic diuresis -> dehydration
3) . peripheral lipolysis -> increased FFAs -> converted to acidic ketones in liver
4) . ketones increase acidity of blood -> metabolic acidosis

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54
Q

DIABETIC KETOACIDOSIS - list 7 clinical features

A

1) . dehydration
2) . vomiting / abdo pain
3) . sunken eyes / dry tongue
4) . Kussmaul’s breathing
5) . fruity breath (ketone smell)
6) . low BP
7) . low temp

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55
Q

DIABETIC KETOACIDOSIS - what’s Kussmaul’s breathing

A
  • deep and rapid breathing

- resp compensation for the metabolic acidosis

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56
Q

DIABETIC KETOACIDOSIS - how would you diagnose (4 things)

A
  • ketones raised
  • blood glucose >11mmol/L
  • blood pH <7.3
  • blood bicarb <15
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57
Q

DIABETIC KETOACIDOSIS - list 3 treatments

A
  • fluid replacement -> 0.9% NaCl (saline)
  • IV insulin
  • electrolytes (k+)
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58
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE - what is it

A
  • complication of DM - high blood sugar -> high osmolarity (lots of particles in solution)
  • little/no ketoacidosis
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59
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE - what causes it

A

infection, especially pneumonia

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60
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE - list 3 clinical features

A
  • dehydration (from osmotic diuresis)
  • reduced consciousness (from conc. plasma)
  • polyuria
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61
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE - how to diagnose

A

blood glucose test

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62
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE - list 4 treatments

A

1) . low molecular weight heparin (hyperosmolality makes blood thick so reduces clots / MI / stroke risk)
2) . fluid replacement 0.9% NaCl
3) . insulin
4) . electrolytes (k+)

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63
Q

Define HYPOTHYROIDISM

A

Reduced action of thyroid hormone

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64
Q

define PRIMARY HYPOTHYROIDISM

A
  • decreased levels of T4

- issue with thyroid gland

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65
Q

define SECONDARY HYPOTHYROIDISM

A
  • decreased TSH

- pituitary / hypothalamic issue

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66
Q

list 4 causes of PRIMARY HYPOTHYROIDISM

A

1) . Primary atrophic hypothyroidism
2) . Hashimoto’s Thyroiditis (autoimmune)
3) . Drugs -> post-thyroidectomy/radioiodine/antithyroid
4) . lithium/amiodarone

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67
Q

list 4 causes of SECONDARY HYPOTHYROIDISM

A

1) . hypopituitarism (neoplasm, infection)
2) . isolated TSH deficiency
3) . hypothalamic disorders (neoplasms, trauma)
4) . iodine deficiency

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68
Q

outline the pathology of PRIMARY HYPOTHYROIDISM

A
  • aggressive autoimmune destruction of thyroid cells

- antibodies bind and block TSH receptors -> inadequate thyroid hormone made/secreted

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69
Q

outline the pathology of SECONDARY HYPOTHYROIDISM

A
  • release + production of TSH is decreased

- therefore reducd T3/T4 released

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70
Q

list 10 symptoms of HYPOTHYROIDISM

A
  • everything down*
    1) . hoarse voice
    2) . constipation
    3) . COLD intolerance
    4) . weight GAIN
    5) . menorrhagia (heavy period)
    6) . myalgia (muscle pain)
    7) . weakness
    8) . tired
    9) . LOW mood
    10) . dementia
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71
Q

list the 11 signs of HYPOTHYROIDISM (think BRADYCARDIC)

A 
Bradycardic(slow HR)
Reflexes relax slowly
Ataxia
Dry thin hair/skin 
Yawning (drowsy/coma)
Cold hands
Ascites (abdo fluid buildup)
Round puffy face
Defeated demeanour 
Immobile 
Congestive heart failure
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72
Q

list 4 investigations for HYPOTHYROIDISM

A

1) . thyroid function test
2) thyroid antibodies
3) . lipids/cholesterol
4) . FBC

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73
Q

what would thyroid function test show in suspected HYPOTHYROIDISM

A

Primary - high TSH / low free T4

Secondary - low TSH / low T3/T4

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74
Q

what would thyroid antibody test show in suspected HYPOTHYROIDISM

A

thyroid antibodies present

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75
Q

what would FBC / cholesterol test show in suspected HYPOTHYROIDISM

A

FBC

  • anaemia
  • macrocytic anaemia in women due to menorrhagia

cholesterol
- hyperlipidemia

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76
Q

outline the management of HYPOTHYROIDISM

A
  • Levothyroxine (T4 replacement)

Primary -> remove thyroid growth (goitre)

Secondary -> treat underlying cause (TSH may always be low)

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77
Q

define HYPERTHYROIDISM (thyrotoxicosis)

A

Overactivity of the thyroid gland -> excess thyroid hormone

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78
Q

list 6 causes of HYPERTHYROIDISM

A

1) . Graves’ disease (most common)
2) . toxic multinodular goitre
3) . toxic thyroid adenoma
4) . pituitary adenoma
5) . De Quervain’s thyroiditis
6) . Iatrogenic -> iodine/amiodarone/lithium

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79
Q

what is De Quervain’s thyroiditis

A
  • short lasting hyperthyroidism
  • accompanied by:
    1) .fever
    2) .malaise
    3) .neck pain
  • treat with aspirin
  • give prednisolone if severe
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80
Q

list 9 symptoms of HYPERTHYROIDISM

A
  • everything UP*
    1) . Palpitations
    2) . diarrhoea
    3) . HEAT intolerant
    4) . weight LOSS
    5) . INCREASED appetite
    6) . oligomenorrhea
    7) . tremor
    8) . irritable
    9) . Labile emotion (volatile)
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81
Q

list 11 signs of HYPERTHYROIDISM (6 categories)

A 
HANDS - moist/warm/red palms
PULSE - tachycardic/AF
FACE - thin hair
NECK - Goitre/nodules/bruit
SWEATING
HYPERREFLEXIA
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82
Q

list 4 investigations for suspected HYPERTHYROIDISM

A

1) .Thyroid function tests
2) . thyroid autoantibodies
3) . thyroid ultrasound
4) . radioactive iodine isotope uptake scan

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83
Q

what would be the results of TFTs in suspected HYPERTHYROIDISM

A

Primary

  • low TSH
  • high T3/T4

Secondary

  • high TSH
  • high T3/T4
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84
Q

what would be the results of thyroid autoantibodies in suspected HYPERTHYROIDISM

A
  • TPOs more often seen in HYPOTHYROIDISM
  • thyroglobulin antibodies seen
  • TSH receptor antibody (TRAb) in GRAVES’
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85
Q

what would be the results of radioactive iodine uptake scan in HYPERTHYROIDISM

A
  • much greater uptake of iodine in GRAVES’
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86
Q

list 4 treatments HYPERTHYROIDISM

A

1) . beta blockers
2) . anti-thyroid drug
3) . radioiodine therapy
4) . thyroidectomy

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87
Q

drug class - BETA BLOCKER. give example + method of action

A
  • PROPRANOLOL
  • rapidly controls symptoms
  • decreases Sympathetic Nervous System (SNS)
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88
Q

drug class - ANTI-THYROID. give example + method of action

A
  • CARBIMAZOLE
  • blocks thyroid hormone synthesis
  • has immunosuppressive effects which affect GRAVES’
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89
Q

Contraindications and side effects of RADIOIODINETHERAPY

A

CI

  • pregnancy
  • breast feeding

SE
- Lead to HYPOTHYROIDISM

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90
Q

list 3 potential complications of THYROIDECTOMY

A

1) bleeding
2) post-op infection
3) hypothyroidism

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91
Q

define GRAVES’ disease

A
  • hyperthyroidism

- due to pathological stimulation of TSH receptor

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92
Q

list a cause of GRAVES’

A
  • autoimmune disease

- associated with mysthenia gravis

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93
Q

list 5 signs / symptoms of GRAVES’

A

1) . increased HR
2) tremor
3) NECK - goitre/brut
4) EYES - bulging out/proptosis
5) Thyroid ACROPACHY (swelling of hands/feet)

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94
Q

Investigation for GRAVES’

A

TFTs

  • high T3/T4
  • Low TSH
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95
Q

outline management for GRAVES’

A

same as HYPERTHYROIDISM

1) . Beta blocker
2) . anti-thyroid drug
3) . thyroidectomy
4) radioiodine therapy

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96
Q

define HASHIMOTO’S THYROIDITIS

A
  • hypothyroidism

- due to aggressive thyroid cell destruction

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97
Q

epidemiology of HASHIMOTO’S THYROIDITIS (3 things)

A

1) . 12-20x more common in women
2) . most common cause of goitrous hypothyroidism
3) . associated with other autoimmune conditions

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98
Q

cause of HASHIMOTO’S THYROIDITIS + 3 triggers

A

autoimmune

Triggers

1) . iodine
2) . infection
3) . smoking

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99
Q

pathology of HASHIMOTO’S THYROIDITIS

A

1) . aggressive autoimmune destruction of thyroid cells
2) . antibodies bind and block TSH receptors
3) . blocking leads to inadequate thyroid hormone production/scretion

100
Q

list 4 signs / symptoms of HASHIMOTO’S THYROIDITIS

A

1) hypothyroid symptoms
2) . rapidly enlarged thyroid gland
3) . dyspnoea / dysphagia (from neck pressures)
4) . Goitre

101
Q

list 2 investigations and what you’d see in suspected HASHIMOTO’S THYROIDITIS

A

1) . TFTs
- TSH raised

2) . Thyroid antibodies
- present

102
Q

3 ways to manage HASHIMOTO’S THYROIDITIS

A

same as hypothyroidism

1) . levothyroxine
2) . remove goitre
3) . treat underlying cause

103
Q

list 5 thyroid cancers in order of prevalence

A
  • all different cell types*
    1) . papillary
    2) . follicular
    3) . medullary
    4) . lymphoma
    5) . anaplastic
104
Q

describe the behaviour/spread/prognosis for PAPILLARY

A

B). usually effects young people
S). local
P). good

105
Q

describe the behaviour/spread/prognosis for FOLLICULAR

A

B). effects middle aged people
S). lung/bone
P). usually good

106
Q

describe the behaviour/spread/prognosis for MEDULLARY

A

B). often familial
S). local and metastases
P). poor

107
Q

describe the behaviour/prognosis for LYMPHOMA

A

B). variable

P). usually poor

108
Q

describe the behaviour/spread/prognosis for ANAPLASTIC

A

B). aggressive
S). local
P). very poor

109
Q

list 2 signs/symptoms of:

  • PAPILLARY
  • FOLLICULAR
  • ANAPLASTIC
A

1) . hard fixed nodule

2) . enlarged lymph nodes on examination

110
Q

list a sign/symptom of LYMPHOMA

A

rapidly growing mass in neck

111
Q

list 3 signs/symptoms of MEDULLARY

A

1) . diarrhoea
2) . flushing episodes
3) . itching

112
Q

what is the differential for THYROID CANCERS

A

goitre

113
Q

investigation for THYROID CANCERS

A
  • fine needle aspiration (biopsy)
114
Q

what is the management for:

  • PAPILLARY
  • FOLLICULAR
A

TOTAL thyroidectomy (remove whole gland)

115
Q

what is the management for:

  • ANAPLASTIC
  • LYMPHOMA
A

Radiotherapy for palliative care

116
Q

list 2 managements for:

- MEDULLARY

A

1) . TOTAL thyroidectomy

2) . central lymph node dissection

117
Q

define CUSHING’S SYNDROME

A
  • persistently elevated glucocorticoid in circulation (CORTISOL)
118
Q

where is cortisol released

A

Zona Fasciculata of adrenal gland

119
Q

epidemiology of CUSHING’S

A
  • 2/3rds of cases = Cushing’s Disease

- increased incidence in diabetes

120
Q

list the types of causes for CUSHING’S syndrome

A

1) . ACTH dependant

2) . ACTH independent

121
Q

list 3 causes of ACTH Dependant disease

A

increased Adrenocorticotropic

1) . excessive ACTH from pituitary adenoma (CUSHING’S DISEASE)
2) . ACTH producing tumour
3) excess ACTH administration

122
Q

list 3 causes of ACTH independent disease

A
  • decreased adrenocorticotropic*

1) . adrenal adenoma/carcinoma
2) . adrenal nodular hyperplasia
3) . excess glucocorticoid administration (iatrogenic -> hydrocortisone)

123
Q

what is CUSHING’S DISEASE

A

cushing’s syndrome but cause is PITUITARY ADENOMA

124
Q

outline the pathology of CUSHING’S SYNDROME

A

1) . lots of features bc cortisol is catabolic -> thin skin / easy bruising / striae
2) . excessive alcohol mimics signs (pseudo-cushing’s) -> fixed with alcohol recession
3) . loss of normal feedback mechanisms / loss of circadian rhythm

125
Q

list 6 symptoms of CUSHING’S SYNDROME

A

1) . acne
2) . weight GAIN
3) . gonadal dysfunction (irregular menses/hirsutism/virilisation)
4) . weakness
5) . mood change
6) . recurrent achilles injury

126
Q

briefly outline the gonadal dysfunction seen in CUSHING’S SYNDROME

A

1) . irregular menses (periods)
2) . hirsutism -> hair growing where it shouldn’t
3) . virilisation -> male characteristics developing in a female or too early in a boy

127
Q

list 10 signs of CUSHING’S SYNDROME (3 categories)

A

FAT DISTRIBUTION

  • central obesity
  • moon face
  • buffalo neck hump
  • supraclavicular fat

SKIN CHANGES

  • thin skin
  • bruising
  • purple abdo striae

OTHER

  • osteoporosis
  • red face
  • muscle atrophy
128
Q

outline investigation pathway for CUSHING’S SYNDROME

A

1) . confirm raised cortisol

2) . establish cause (do plasma cortisol)

129
Q

CUSHING’S SYNDROME - investigations to confirm raised cortisol

A

1) . overnight dexamethasone suppression test (shows no suppression)
2) . 48 hour low-dexamethasone suppression test (shows urinary free cortisol elevated)

130
Q

CUSHING’S SYNDROME - investigations to establish cause

A

PLASMA CORTISOL (synacthen)

1) . if ACTH undetectable
- susp adrenal tumour
- CT adrenal glands
- if no mass -> adrenal vein sampling

2) . if ACTH detectable
- pituitary issue or ectopic
- high dose dexamethasone suppression test (pituitary causes suppression)
- CRH test (cortisol rises with pituitary)

131
Q

outline the 5 treatment pathways for CUSHING’S SYNDROME

A

1). stop steroids (iatrogenic)

2). adrenalectomy (adrenal adenoma)
adrenalectomy + radiotherapy + adrenolytic drugs (adrenal carcinoma)

3) trans-sphenoidal surgery / bilateral adrenalectomy (Cushing’s disease)
4) . cortisol synthesis inhibition drugs
5) . surgery to remove tumour (ectopic)

132
Q

list 3 drugs which bring down cortisol levels

A

1) metyrapone
2) ketoconazole
3) fluconazole

133
Q

explain the risk of an adrenalectomy

A

may cause NELSON’S SYNDROME

  • adrenals removed = no cortisol to respond to ACTH
  • no cortisol = no negative feedback loop for ACTH
  • ACTH builds up in tissues

FEATURES

  • bronze skin
  • visual disturbance
  • headache
134
Q

define ACROMEGALY

A
  • overgrowth of all organ systems

- due to excess growth hormone

135
Q

epidemiology of ACROMEGALY

A
  • avg age = 40

- 5% association with MEN-1 (hereditary endo tumours)

136
Q

list 3 causes of ACROMEGALY

A

1) . excessive GH secretion via pituitary tumour
2) . other GH releasing tumours (hypothalamus/lung)
3) . hyperplasia

137
Q

outline the pathology of ACROMEGALY

A
  • GH acts directly on tissues ie. liver/bone/muscle
  • GH acts indirectly via induction of IGF-1 (insulin-like growth factor)
  • excess causes uncontrolled growth
138
Q

how can GIGANTISM occur

A

if ACROMEGALY present in children before epiphyseal plates fuse

139
Q

list 8 symptoms of ACROMEGALY (slow onset)

A

1) . snoring
2) . deep voice
3) . increased sweating
4) . weight GAIN
5) . reduced libido
6) . amenorrhoea
7) . back pain
8) . acroparesthesia (burning/tingling in extremities when you wake up)

140
Q

list 6 signs of ACROMEGALY

A

1) skin darkening - acanthosis nigricans
2) prognathism (jaw protrudes)
3) . interdental separation (gap teeth)
4) . macroglosia (huge tongue)
5) . spade hands/feet
6) . carpal tunnel syndrome

141
Q

list 4 investigations and what you’d expect to see in ACROMEGALY

A

1) . oral GTT = GH high after given glucose
2) . serum IGF-1 = raised IGF-1
3) . MRI pituitary fossa = evidence of pituitary adenoma
4) . visual field test = bitemporal hemianopia

142
Q

why shouldn’t you rely on just a random Growth Hormone test for ACROMEGALY

A
  • GH has pulsatile secretion

- levels vary throughout the day

143
Q

outline the 1st/2nd/3rd line management for ACROMEGALY

A

1st line
- transphenoidal resection surgery (removes adenoma / corrects surroundings)

2nd line
- somatostatin analogues
(octreotide)

3rd line
- GH receptor antagonists
(pegvisomant)

144
Q

list 3 complications of ACROMEGALY

A

1) . hypertension
2) . diabetes
3) . untreated can impact optic chiasm -> blindness

145
Q

define CONN’S SYNDROME (primary hyperaldosteronism)

A
  • high aldosterone levels
  • independant of RAAS
  • Na / water retention
146
Q

list 2 causes of CONN’S SYNDROME

A

1) . adrenal adenoma -> secreting aldosterone

2) . bilateral adrenal hyperplasia

147
Q

outline the pathology of CONN’S SYNDROME

A

1) aldosterone causes Na/K exchange in distal renal tubule
2) . therefore hyperaldosteronism causes increased Na/water resorption
- and also causes increased K excretion
3) . reduced renin release

148
Q

list 6 signs and symptoms for CONN’S SYNDROME

A
  • HYPOKALAEMIC signs*
    1) . cramps
    2) . alkalosis
    3) . weakness
    4) . hypertension

ALSO

1) . low urine output
2) . paraesthesia(pins/needles)

149
Q

outline the 3 tests for CONN’S SYNDROME and what each would show

A

U&E’s

1) decreased renin
2) increased aldosterone
3) Na = UP
4) K = DOWN

ECG

1) flat T wave
2) ST depression
3) long QT
4) long PR
5) pathological U wave

Adrenal CT/MRI
- confirmation of aldosterone producing adenoma

150
Q

outline the 2 treatments for CONN’S SYNDROME

A

if ADENOMA
- laparascopic adrenalectomy

if HYPERPLASIA
- aldosterone antagonist
( spironolactone)

151
Q

define ADDISON’S DISEASE

A
  • primary adrenocortical insufficiency
  • destruction of adrenal cortex
  • decrease in gluco/mineralocorticoids/androgens
152
Q

outline the pathology of ADDISON’S DISEASE

A

1) . destruction of adrenal cortex
2) . less cortical produced
3) . excess ACTH stimulates melanocytes
4) . hyperpigmentation

153
Q

list 4 causes of ADDISON’S DISEASE

A

1) . autoimmune adrenalitis
2) . adrenal TB
3) . surgical removal of adrenals
4) . adrenal metastases

154
Q

list 12 symptoms of ADDISON’S DISEASE (4 categories)

Tanned, tired, toned, tearful

A

GI

1) . nausea/vomiting
2) . abdo pain
3) . constipation/diarrhoea
4) . anorexia

BODY

1) . tanned skin
2) . lean -> weight loss

NEURO

1) . weakness
2) . confusion
3) . syncope (faint)

OTHER

1) . myalgia (tired muscles)
2) . depression
3) . malaise (discomfort)

155
Q

list 8 signs of ADDISON’S DISEASE (3 categories)

A

HYPERPIGMENTATION

1) . palmar creases
2) . buccal mucosa (brown mouth)
3) . vitiligo (patchy skin)

CARDIO

1) . postural hypotension (BP drops when stood up)
2) . shock BP up/HR down/coma

OTHER

1) . dehydration
2) . general wasting
3) . alopecia

156
Q

outline the 4 investigations and what you’d see for ADDISON’S DISEASE

A

1) . ACTH stimulation test
- cortisol stays low after giving ACTH (synACTHen)

2) . plasma ACTH
- HIGH = primary hypoaldosteronism
- LOW = secondary/tertiary hypoaldosteronism

3) . U&E
- high renin
- low aldosterone
- low Na
- high K
- high urea

4) . adrenal antibodies
- 21-hydroxylase present

157
Q

outline the 3 treatments for ADDISON’S DISEASE

A

1) . Replace glucocorticoids (cortisol) with Hydrocortisone/Prednisolone
2) . replace mineralocorticoids (aldosterone) with fludrocortisone
3) . double dose of steroids if infection/trauma/surgery

158
Q

what is the function of potassium K+

A

maintains resting potential of all muscles in body

159
Q

give 3 ways that serum potassium K+ is controlled

A

1) . uptake of K+ into cells
2) . renal excretion (aldosterone)
3) . GI loss

160
Q

define HYPERKALEMIA

A

abnormally high potassium K+ in blood

161
Q

list 5 causes of HYPERKALEMIA (think DREAD)

A 
Drugs (ACE-i/K+ sparing diuretics)
Renal failure 
Endocrine (Addison's)
Artefact (consider ECG)
DKA (or other acidosis)
162
Q

outline the pathology of HYPERKALEMIA

A

1) . K+ in blood determines excitability of nerve and muscle cells including heart
2) . when K+ rises -> reduced electrical potential btwn cardiac myocyte/outside cell
3) . threshold for action potential decreased
4) . abnormal action potential -> arrhythmias -> cardiac arrest

163
Q

list 6 Symptoms + 2 Signs of

HYPERKALEMIA

A

SYMPTOMS

1) . usually asymptomatic til reaches MI
2) . muscle weakness
3) . impaired neuromuscular transmission
4) . flaccid paralysis
5) . light headed
6) . chest pain

SIGNS

1) . tachycardia
2) . Kussmaul’s breathing (from metabolic acidosis)

164
Q

outline 2 investigations for HYPERKALEMIA and what you would see

A

U&Es
>5.5mmol/L = hyperkalaemic
>6.5mmol/L = emergency

ECG

  • tall tented T waves
  • Small P waves
  • Wide QRS complex
165
Q

outline 4 treatments for MILD HYPERKALEMIA

A

1) . treat underlying cause
2) . dietary Potassium restriction
3) . restrict hypokalaemic drugs
4) . loop diuretic

166
Q

example of loop diuretic and how it works

A
  • FUROSEMIDE

- increases urinary k+ excretion

167
Q

outline 1st/2nd/3rd line treeatment for SEVERE HYPERKALEMIA (medical emergency)

A

1st) . Calcium Gluconate (stabilise cardiac membrane)
2nd) . insulin + dextrose (drive K+ into cells)
3rd) . polystyrene sulfonate resin (binds K+ in gut = decreased uptake)

168
Q

define HYPOKALEMIA

A

deficiency of potassium K+ in blood stream

169
Q

outline tha pathology of HYPOKALEMIA

A

1) . low K+ in serum (ECF)
2) . causes water conc. grad out of cell (ICF)

3) . increased leakage from ICF
4) . cardiac myocyte membrane hyperpolarised
5) . monocyte excitability decreased

170
Q

list 5 causes of HYPOKALEMIA

A

1) . fasting
2) . anorexia
3) . high renal aldosterone (aldosterone stimulates K+ excretion)
4) . increased renal excretion (loop diuretics)
5) . GI loss (vomiting/diarrhoea)

171
Q

list 5 signs/symptoms of HYPOKALEMIA

A

usually asymptomatic

1) . muscle weakness
2) . cramps
3) . tetany (intermittent muscle spasms)
4) . palpitations
5) . constipation

172
Q

list 2 investigations and their findings for HYPOKALEMIA

A

U&E (serum K+)
<3.5mmol/L = hypokalaemia
<2.5mmol/L = emergency

ECG

1) . U waves
2) . small/inverted T
3) . ST depression
4) . long PR
5) . long QT

173
Q

outline the treatment for mild and severe HYPOKALEMIA

A

MILD

  • Oral K+ (sando-K)
  • K+ sparing diuretic (spironolactone)

SEVERE
- IV K+

174
Q

define SYNDROME OF INAPPROPRIATE ADH (SIADH)

A
  • continued ADH secretion

- despite plasma hypotonicity and normal plasma volume

175
Q

what’s the generalised cause of SIADH

A
  • disordered hypothalamic-pituitary secretion

- ectopic production of ADH

176
Q

List 3 Neuro causes of SIADH

A

1) tumour
2) trauma
3) meningitis

177
Q

List 3 Pulmonary causes of SIADH

A

1) .Cystic Fibrosis
2) . Asthma
3) . Pneumonia

178
Q

List 4 Drug causes of SIADH

A

1) . opiates
2) . carbamazepine
3) . chloropropamide
4) . vincristine

179
Q

List 4 Malignancy causes of SIADH

A

1) . small cell lung carcinoma
2) . prostate
3) .thymus
4) pancreas

180
Q

outline the pathology of SIADH

A

excess ADH -> more aquaporin 2 inserted -> water retention -> excess blood volume -> hyponatremia (via dilution)

181
Q

list 5 symptoms for SIADH

A

1) . Reduced GCS (confused/drowsy)
2) . irritable
3) . headaches
4) . anorexia
5) . Nausea

182
Q

list 2 signs of SIADH

A

1) . conc urine

2) . dilutional hyponatremia -> leads to fits/coma

183
Q

describe 3 tests for SIADH and what they’d show

A

U&E
- dilutional hyponatraemia (low Na)

Osmolality
- low plasma osmolality

Urinalysis
- Urinary Na secretion

184
Q

outline 4 management strategies for SIADH

A

1) . treat underlying cause
2) . restrict fluid (increases Na+ conc)

3) . DEMECLOCYCLINE
- inhibit ADH action on kidneys
- causes Diabetes insipidus

4) . TOLVAPTAN
- vasopressin receptor antagonist
- V2 blocker

185
Q

define DIABETES INSIPIDUS

A

lack of ADH

Neurogenic = hyposecretion
Nephrogenic = insensitivity
186
Q

list 5 Neurogenic causes of DIABETES INSIPIDUS

A

NEUROGENIC

1) . idiopathic
2) . tumour
3) . neurosurgery
4) . ADH gene mutation
5) . infection (TB)

187
Q

list 5 Nephrogenic causes of DIABETES INSIPIDUS

A

NEPHROGENIC

1) . chronic renal disease
2) . drugs (lithium)
3) . hypercalcemia
4) . hypokalemia
5) . ADH receptor mutation

188
Q

Outline the pathology of NEUROGENIC DIABETES INSIPIDUS

A

1) . disease of hypothalamus -> insufficient ADH made

2) . damage to post pituitary doesn’t affect it as ADH can still leak out

189
Q

Outline the pathology of NEPHROGENIC DIABETES INSIPIDUS

A

1) . channel disruption

2) . kidney damage -> doesn’t respond to ADH

190
Q

list 5 signs/symptoms of DIABETES INSIPIDUS

A

1) . polydipsia
2) . polyuria
3) . dehydration
4) . hypernatremia
5) . nocturia

191
Q

list 4 investigations and what you would see for - Nephrogenic = osmolarity still low after adding DESMOPRESSIN (ADH analogue)
- Neurogenic = back to normal with DESMOPRESSIN

A

WATER DEPRIVATION TEST
- urine osmolarity low (diluted) after fluid restricted

MRI HYPOTHALAMUS
- confirms DI

URINE VOLUME
- high urine volumes confirm plyuria

U&E
- rule out more common issue

192
Q

Changes to Water Deprivation Test to differentiate btwn neuro/nephrogenic DIABETES INSIPIDUS

A

Nephrogenic = osmolarity still low after adding DESMOPRESSIN (ADH analogue)
- Neurogenic = back to normal with DESMOPRESSIN

193
Q

management for NEUROGENIC DIABETES INSIPIDUS

A

ADH analogue

- Desmopressin

194
Q

2 managements for NEPHROGENIC DIABETES INSIPIDUS

A

1) . Thiazide diuretics

2) . NSAIDs

195
Q

Give example of 2 thiazide diuretics and how they works

A

1) .Bendroflumethiazide
2) .Hydrochlorothiazide

  • increased Na+ secretion in DCT -> increased water loss -> body reduces GFR
196
Q

how do NSAIDs work in treating NEPHROGENIC DIABETES INSIPIDUS

A
  • inhibit prostaglandin synthase -> less prostaglandins -> reduced local ADH inhibition
197
Q

Explain how the Parathyroid gland controls Calcium balance

A

releases PTH -> more calcium

1) . stimulates kidneys / GI tract to absorb more calcium
2) . stimulates osteoclasts to break down bones and released stored calcium
3) . increases Calcitriol levels (active Vit D) which increases GI/Kidney absorption of calcium

198
Q

Explain how the Thyroid gland controls Calcium balance

A

releases CALCITONIN -> less calcium

1) . thyroid receptors stimulated when calcium gets too high
2) . this causes release of calcitonin
3) . calcitonin inhibits GI resorption
4) . calcitonin increases osteoblast activity

199
Q

define HYPOCALCAEMIA

A

low serum calcium

200
Q

list 5 causes of HYPOCALCEMIA

A

1). Actual Vit D deficiency (diet/sunlight/malabsorption)
2). Functional Vit D deficiency
(renal = no 1-hydroxylation)
(liver = no 25-hydroxylation)
3). Hypoparathyroidism
4). osteomalacia
5). Chronic Kidney Disease

201
Q

outline the pathology of HYPOCALCAEMIA

A

CKD

1) poor renal calcium uptake
2) due to low active vit D production + renal phosphate retention
3) microprecipitation of calcium phosphate in tissues

202
Q

5 symptoms of HYPOCALCAEMIA

A

1) . Spasms (Hands/feet/larynx/uterus)
2) . peripheral paraesthesia
3) . anxious
4) . seizures
5) . muscle tone UP

203
Q

list 4 signs of HYPOCALCAEMIA

A

1) . convulsion
2) . arrhythmia
3) Chvostek’s sign
4) . Trousseau’s sign

204
Q

what is Chvostek’s sign

A
  • tap over facial nerve where parotid gland is

- causes twitching of ipsilateral facial muscles

205
Q

what is Trousseau’s sign

A
  • carpopedal spasm (hands/feet)

- induced by inflating BP cuff 20mmHg > systolic BP

206
Q

outline the SPASMODIC mnemonic for signs / symptoms of HYPOCALCAEMIA

A 
Spasms (Trousseaus)
Paraesthesia
Anxious
Seizure
Muscle tone up
Orientation impaired
Dermatitis (eczema)
Impetigo
Chvostek's sign
207
Q

list 3 investigations and what you would see for HYPOCALCAEMIA

A

ECG
- long QT

FBC
- PTH high

eGFR
- search for CKD

208
Q

treatment for mild HYPOCALCAEMIA

A

Adcal supplement

209
Q

treatment for severe HYPOCALCAEMIA

A

calcium gluconate

210
Q

define HYPERCALCAEMIA

A

high serum calcium

211
Q

2 causes of HYPERCALCAEMIA

A

1) . primary hyperparathyroidism

2) . malignancy

212
Q

outline the pathology of HYPERCALCAEMIA

A

ectopic secretion of PTH is rare

MALIGNANCY

  • works by secreting PTH like peptide
  • directly invades bone and produces local factors to mobilise calcium (unregulated bone breakdown)
213
Q

list 10 symptoms of HYPERCALCAEMIA (Bones/Stones/Moans/Groans)

A

BONES

1) . painful bone condition
- osteitis fibrosa cystica

STONES
2). Ca deposition in renal tubules -> polyuria / nocturia. can lead to CKD

MOANS (Psych issues)

3) . lethargy
4) . depression
5) . psychosis
6) . memory loss
7) . fatigue

GROANS

8) . abdo pain
9) . nausea
10) . constipation

214
Q

2 signs of HYPERCALCAEMIA

A

1) . polyuria

2) . polydipsia

215
Q

2 investigations for HYPERCALCAEMIA

A

ECG
- short QT

FBC
- raised calcium

216
Q

outline 3 treatments for HYPERCALCAEMIA

A

1) . loop diuretics -> return calcium to normal
2) . if primary hyperparathyroidism -> surgical removal of parathyroid adenoma
3) . IV bisphosphonates -> make osteoclasts apoptose to reduce bone resorption

217
Q

define HYPERPARATHYROIDISM

A

excess PTH secretion

218
Q

list 2 causes for PRIMARY HYPERPARATHYROIDISM

A

1) . single parathyroid adenoma

2) . hyperplasia

219
Q

outline the pathology of PRIMARY HYPERPARATHYROIDISM

A
  • adenoma / hyperplasia provides extra secretive tissue

- excess PTH made

220
Q

list the symptoms for HYPERPARATHYROIDISM (4 categories!)

A

same as hypercalcemic

BONES
- pain

STONES
- renal/biliary stones

ABDO GROANS

  • nausea
  • vomiting
  • constipation
  • indigestion

PSYCH MOANS

  • fatigue
  • depression
  • psychosis
  • memory loss
  • lethargy
221
Q

list 3 investigations for HYPERPARATHYROIDISM

A

1) . FBC
2) . DEXA bone scan for osteoporosis
3) . Abdo X-RAY for renal calculi

222
Q

what blood results would you see in PRIMARY HYPERPARATHYROIDISM

A
  • Ca high
  • PTH high
  • phosphate low
223
Q

list 4 signs for HYPERPARATHYROIDISM

A

1) . fractures
2) . pain
3) . osteoporosis
4) . hypertension

224
Q

management for PRIMARY HYPERPARATHYROIDISM

A

1) . if adenoma - surgical removal
2) . if hyperplasia - remove all 4 glands
3) . Calcimimetic (cinacalcet)

225
Q

give example of calcimimetic and how it works

A

CINACALCET

  • increase parathyroid cell sensitivity to Ca2+
  • so less PTH secreted
226
Q

list 3 causes of SECONDARY HYPERTHYROIDISM

A

1) . CKD
2) . low vit D
3) . malabsorption (any hypocalcemic disease)

227
Q

outline pathology of SECONDARY HYPERTHYROIDISM

A

parathyroid gland becomes hyperplastic to compensate for chronic hypocalcemia

228
Q

what would you see in bloods for SECONDARY HYPERTHYROIDISM

A
  • Ca low
  • PTH high
  • phosphate high
229
Q

management of SECONDARY HYPERTHYROIDISM

A
  • treat underlying cause
230
Q

cause of TERTIARY HYPERTHYROIDISM

A

develops from secondary hypoparathyroidism (CKD)

231
Q

explain the pathology of TERTIARY HYPERTHYROIDISM

A
  • glands become autonomous

- produce excess PTH even when calcium deficiency corrected

232
Q

what would you see in bloods for TERTIARY HYPERTHYROIDISM

A
  • Ca high
  • PTH high
  • phosphate high
233
Q

list 2 managements for TERTIARY HYPERTHYROIDISM

A

1) . calcium mimetic (cincalcet)

2) . parathyroidectomy

234
Q

complication of PRIMARY HYPERTHYROIDISM if not treated

A

hypercalcemia

235
Q

complication of SECONDARY HYPERTHYROIDISM if not treated

A

develops into tertiary hyperparathyroidism

236
Q

complication of parathyroidectomy

A

transient hypocalcaemia

237
Q

define HYPOPARATHYROIDISM

A

low levels of PTH

238
Q

list 4 causes of HYPOPARATHYROIDISM

A

1) . could be transient
2) . common after anterior neck surgery
3) . genetic -> PTH gene defect
4) . autoimmune (Di-George)

239
Q

outline the pathology of HYPOPARATHYROIDISM

A

1) . PTH normally stimulates vit D activation
2) . low PTH present means vit D functions don’t occur
3) . result is hypocalcemia / hyperphosphatemia

240
Q

list 4 functions of activated Vit D

A
  • GI calcium absorption
  • renal calcium absorption
  • calcium release from bone
  • inhibit phosphate reabsorption
241
Q

list 6 symptoms of HYPOPARATHYROIDISM

A

same as hypocalcaemia

1) . increased excitability of muscles/nerves
2) . mouth/extremity paresthesia
3) . cramps
4) . convulsions
5) . tetany
6) . increased reflexes

242
Q

2 signs for HYPOPARATHYROIDISM

A

same as hypocalcemia

1) . Chvostek’s (twitching facial muscles over)
2) . Trousseau’s (cardopedal spasm)

243
Q

2 investigations for HYPOPARATHYROIDISM and the results

A

FBC

  • Ca low
  • PTH low
  • phosphate high

ECG

  • long QT
  • HR / conctractility down
244
Q

treatment for acute and persistent HYPOPARATHYROIDISM

A

ACUTE
- IV calcium

PERSISTENT
- Vit D analogue (alfacalcidol)

245
Q

complication of treating HYPOPARATHYROIDISM

A
  • could over treat with vit D

- leads to hypercalcemia

Phase 2a Medicine (2 decks)

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