Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > Endocrinology Conditions > Flashcards

Endocrinology Conditions Flashcards

1
Q

Diabetes Mellitus - Describe the clinical presentation (of young and old patients)

A

Young: 2-6 week history of thirst, polyuria and weight loss. Ketoacidosis if not picked up earlier (fruity breath). Older: Similar, but over longer period. Additionally lack of energy and eye problems (blurred vision). Neuropathy, eventually (glove and stockings). Exist on a spectrum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diabetes Mellitus - Type 1 Pathophysiology

A

Caused by an autoimmune destruction of the pancreatic beta cells. Associated with HLA genetics (>90% with HLA-DR3/4 genes are affected) but triggered by environmental antigens. Will have the autoantibodies (bad ones) several years before onset.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diabetes Mellitus - Type 1 Pathophysiology of Polyuria

A

Renal glucose reabsorption cannot retrieve the amount of glucose that was filtered out of the blood and so it increases urea output (osmotic diuresis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diabetes Mellitus - Type 1 Pathophysiology of Weight Loss

A

Fluid depletion and insulin deficiency leads to muscle and fat breakdown.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diabetes Mellitus - Type 2 Pathophysiology

A

Polygenic (not HLA related). Environmental factors trigger onset in the genetically susceptible.

Peripheral insulin resistance caused by the receptors that insulin acts on being overused so they don’t bind as well. After a while beta cell mass reduces, insulin secretion reduces and you can get pancreatic failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diabetes Mellitus - Type 2 causes (5)

A

Cushing’s disease, acromegaly, hyperthyroidism, pregnancy, pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Diabetes Mellitus - Type 1 Epidemiology

A

Onset usually <30 years. Usually fairly thin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diabetes Mellitus - Type 2 Epidemiology

A

Onset usually >30 years. Usually overweight.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diabetes Mellitus - Investigations with results (4)

A

Test fasting glucose (not eaten for 8 hours), >7 mmol/L is positive.

Random glucose >11.1 mmol/L is positive.

HbA1c needs 6.5%/48mmol/mol

Low C peptide in type 1

Normal C peptide in type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diabetes Mellitus - Type 1 Treatment (3)

A

Glycaemic control through diet (low sugar, low fat, high starch) and insulin (twice daily and with meals)

Basal insulin - long acting insulin, lasts for 12-24 hours. Mixed with protamine or zinc

Bolus insulin - short acting soluble insulins work within 30-60 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diabetes Mellitus - Type 2 Treatment (5)

A

Diet and exercise.

If that doesnt work use metformin, gliclazide, sitagliptin or insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diabetes Mellitus - Pharmacology (Drug class, example, mechanism of action, side effects 4)

A
  • Biguanide, Metormin, Reduce gluconeogenesis in liver, increase glucose upatke in skeletal muscle, GI - abdo pain, anorxia, diarrhoea, neusea, Lactic acidosis
  • Sulfonylurea, Gliclazide/Glipizide, Stimulate B cells to secrete insulin, Hypoglycaemia, weight gain
  • DPP4 Inhibitors, Sitagliptin, Inhibits DPP4 which stimulates insulin secretion, no weight implications
  • Glitazone, Pioglitazone, Enhance uptake of fatty acids and glucose, Fluid retention, wieght gain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diabetes Mellitus - List Complications (7)

A
  • Hypoglycaemia
  • Diabetic Ketoacidosis
  • Hyperglycaemic hyperosmolar state
  • Diabetic neuropathy
  • Diabetic foot
  • Diabetic retinopathies
  • Diabetic nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diabetes Mellitus - Describe the normal insulin secretion process

A
  • Hyperglycaemia leads to increase glucose uptake by cells
  • Glucose metabolism leads to increased levels of ATP within cell
  • Increased ATP causes K+ channels to close
  • Causes depolarisation of cell membrane
  • Ca2+ channels open and Ca2+ enters cells
  • Increased Ca2+ causes exocytosis of insulin containing vesicles in pancreatic beta cells in the islets of langerhans and insulin in released.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diabetes Mellitus - Hypoglycaemia (definition, symptoms 5, investigations, management)

A
  • Insufficient glucose to the brain
  • Aggression, sweating, tachycardia, hunger, pallor
  • Blood glucose level test (<4mmol/L)
  • Give glucose and glucagon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diabetes Mellitus - Diabetic Ketoacidosis pathology

A
  • Without insulin there is increased hepatic gluconeogenesis
  • High glucose leads to osmotic diuresis leading to dehydration
  • Peripheral lipolysis increases circulating FFAs which are converted to acidic ketones in the liver
  • Process is accelerated by stress hormones secreted because of dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diabetes Mellitus - Diabetic Ketoacidosis Symptoms (5)

A
  • Dehydration
  • Vomiting and abdominal pain (electrolyte disturbances)
  • Low BP
  • Fruity breath (smells of ketones)
  • Low body temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diabetes Mellitus - Diabetic Ketoacidosis Investigations (4)

A
  • Blood tests for hyperglycaemia - blood glucose >11 mmol/L
  • Ketonaemia - blood ketones
  • Urine dipstick
  • Serum U+E - urea and electrolytes. Urea raised, potassium low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diabetes Mellitus - Diabetic Ketoacidosis Treatment (3)

A
  • Fluid replacement
  • IV insulin
  • Electrolytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diabetes Mellitus - Hyperglycaemic Hyperosmolar State (description, symptoms 3, investigations, treatment)

A
  • Characterised by hyperglycaemia, hyperosmolality and no ketosis
  • Dehydration (osmotic diuresis), decreased consciousness (elevated plasma osmolality), polyuria
  • Blood glucose level test (>40mmol/L)
  • Fluid replacement, IV insulin, Electrolytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diabetes Mellitus - Diabetic Neuropathy (description and symptoms 4)

A

Occlusion of the vasa nervorum and accumulation of fructose and sorbitol
- Glove and stocking sensation loss
- Hypersensitivity
- Muscle weakness
- Hyporeflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diabetes Mellitus - Diabetic foot (description, clinical presentation, treatment 3)

A
  • Infection, ischaemia and neuropathy lead to tissue necrosis.
  • Reduced sensation, signs of vascular disease in lower leg (thin skin, no hair, bluish)
  • Swab for bacteria, local wound care, reconstructive vascular surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diabetes Mellitus - Diabetic Retinopathies (description, symptoms 6, investigation)

A
  • Too much glucose in the blood causes glucose uptake into lens and blockages of the retinal blood vessels.
  • Spots in vision, blurred vision, fluctuating vision, impaired colour vision, dark areas in vision, vision loss
  • Fundoscopy (cotton wool spots and flare haemorrhages)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diabetes Melllitus - Diabetic Retinopathies Non-proliferative pathophysiology

A
  • Retinal blood vessel walls weaken, microaneurysms leak into retina
  • Large vessels dilate
  • Retinal nerve fibres may swell
  • Macular oedema may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Diabetes Melllitus - Diabetic Retinopathies proliferative pathophysiology

A
  • Damaged blood vessels close off
  • New abnormal blood vessels grow
  • These can leak into the vitreous humour
  • Scar tissue may cause retina to detach from back of eye
  • Pressure may build up affecting optic nerve (glaucoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Diabetes Mellitus - Diabetic Nephropathy (causes 3, signs, treatment)

A
  • Glomerular disease, ischaemic renal lesions, ascending UTIs
  • Microalbuminuria progressing to intermittent albuminuria and persistent proteinuria
  • BP control (ACE-1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diabetes Mellitus - Other forms (4)

A
  • Mature Onset Diabetes of the Young - rare autosomal dominant form of T2DM affecting young people
  • Latent Autoimmune Diabetes of Adults - form of T1DM with slower progression to insulin dependence later on in life
  • Primary Neonatal Diabetes - Occurs in the first 6-12 months of life
  • Gestational Diabetes - diabetes during pregnancy, usually third trimester
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hyperthyroidism - Epidemiology

A
  • More females than males
  • 2-5% of women
  • Presents between 20-40
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hyperthyroidism - Causes (6)

A
  • Graves’ disease - autoimmune induced excess production of thyroid hormone
  • Toxic multinodular goitre - englarged thyroid gland produces too much thyroid hormone
  • Toxic thyroid adenoma
  • Pituitary adenoma - causes more TSH to be produced
  • De Quervain’s thyroiditis - painful swelling of thyroid gland triggered by a viral infection
  • Drug induced - iodine, amiodarone, lithium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hyperthyroidism - Risk Factors

A
  • Female
  • Family history
  • Stress
  • Smoking
  • Amiodarone (drug)
  • HLA-DR3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hyperthyroidism - Pathology of Graves Disease

A

Serum IgG antibodies called TSH receptor stimulating antibodies bind to TSH receptors on the ethyroid and simulate T3/4 production

This results in excess secretion, hyperplasia of the thyroid follicular cells, hyperthyroidism and goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hyperthyroidism - Symptoms of Graves 4

A

Graves Ophthalmology - extraocular muscle swelling, eye discomfort, lacrimation, diplopia

Pretibial myxoedema - purple lesions on anterolateral shins

Thyroid Acropachy - clubbing, swelling of fingers and toes

Goitre - swollen thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hyperthyroidism - Thyroid tests (primary and secondary results, Graves)

A
  • Primary - low TSH, high T3/4
  • Secondary - high TSH, high T3/4
  • TSH receptory antibodies (Graves)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Hyperthyroidism - Treatment 4

A
  • Beta blockers decrease SNS activation
  • Carbimazole - blocks thyroid hormone synthesis and is immunosuppressive so good for graves. Do it with thyroxine prevents hypo. Side effects - agranulocytosis
  • Radioiodine therapy iodine taken up and local irradiation, the tissue damage causes return to normal function
  • Thyroidectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hyperthyroidism - Thyroid Crisis (description, treatment)

A
  • Rare, life-threatening, can cause hyperpyrexia, tachycardia, restlessness, coma
  • Carbimazole, propranolol, potassium iodine (blocks release of thyroid hormone), hydrocortisone (inhibits peripheral conversion of T4 to T3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Hypothyroidism - Epidemiology

A

Affects females more than males

Affects 0.1-2% of the population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Hypothyroidism - Causes (4)

A
  • Post-partum thyroiditis - following childbirth
  • Autoimmune thyroiditis - anti-thyroid autoantibodies atrophies thyroid (Hashimotos)
  • Drug induced - carbimazole, lithium, amiodarone
  • Hashimoto’s - antibodies attach the thyroid causing inflammation and dysfunction, lowering TS/4 levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hypothyroidism - Symptoms (mneumonic)

A

BRADYCARDIC

Bradycardia

Reflexes relax slowly

Ataxia

Dry, thin hair

Yawning

Cold hands

Ascites

Round puffy face

Defeated demeanour

Immobile

Congestive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hypothyroidism - Investigations (3)

A
  • Thyroid function test - primary (high TSH, low free T4), secondary (low TSH, low T3/4)
  • Thyroid antibodies (TPO in Hashimotos)
  • FBC test for anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Hypothyroidism - Mangement

A

Lifelong oral Levothyroxine (T4), aim to get TSH >0.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Hypothyroidism - Describe Secondary Hypothyroidism

A

Associated with pituitary gland or hypothalamus. Not enough TSH due to hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Cushing’s Disease - Pathology

A

Excess ACTH stimulates excess cortisol or neoplasms in adrenals stimulate zona reticularis to produce more cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cushing’s Disease - Differential diagnosis

A

Pseudo-cushing’s syndrome caused by alcohol excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Cushing’s Disease - Causes

A

Mostly caused by real steroids

ACTH dependent - hypersecretion by pituitary adenoma, ectopic e.g. small cell lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Cushing’s Disease - Symptoms (mneumonic)

A

CUSHING

Cataracts

Ulcers

Striae

Hypertension and hyperglycaemia

Infection

Necrosis

Glucosuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Cushing’s Disease - Investigations (1st line and 2nd line)

A

Random cortisol (if high proceed to first line test)

1st line:

  • Overnight dexamethasone suppression test 24hr (usually suppressed cortisol but if it doesn’t then likely cushings)

2nd line:

  • If no suppression in 1st line do 48hr test
  • If plasma ACTH is low do CT/MRI to detect adenoma or carcinoma.
  • If it is high but supressed = pituitary adenoma
  • High but no suppression = ectopic
47
Q

Cushing’s Disease - Treatment (3)

A
  • Stop steroids
  • Remove pituitary adenoma
  • Radiotherapy on adrenal adenoma
48
Q

Acromegaly - Physiology of growth hormones (including inhibition )

A

Hypothalamus → Growth Hormone Releasing Factor → Pituitary gland → Growth hormone → Liver → Insulin-like Growth Factor 1 → Protein synthesis and Cell Division

Inhibited by somatostatin and high glucose

GH acts on tissues e.g. liver/muscles/bone/fat to change metabolism

IFG-1 increases lipolysis and calcium retention, decreases blood glucose, stimulates hypertrophy and hyperplasia of bone and skeletal muscle

49
Q

Acromegaly - Epidemiology

A

3 per million, mean diagnosis age 40, equally male and female

50
Q

Acromegaly - Causes

A

Benign GH-reducing adenoma

Ectopic GH-releasing hormone forms. Carcinoid tumour (rare)

51
Q

Acromegaly - Risk Factors

A

Multiple endocrine neoplasia-1 (MEN-1)

52
Q

Acromegaly - Pathology

A

Increased GH travels to tissues e.g. liver binding to receptors increasing IF-1

Skeletal and soft tissue growth

53
Q

Acromegaly - Symptoms

A

Local tumour expansion in pituitary causes compression of surrounding structures resulting in headaches and visual field loss

Metabolic effects cause sweating, decreased libido, amenorrhoea/oligomenorrhea

Signs - big hands/feet/jaw, widely spaced teeth, puffy lips/eyelids/skin, deep voice

54
Q

Acromegaly - Investigations (4)

A

Oral glucose tolerance test - should suppress GH if not then his is diagnostic

Serum IF-1 levels (almost always raised and fluctuate less than GH)

MRI for pituitary adenoma

Visual field tests

55
Q

Acromegaly - Treatment

A

1st line - transphenoidal surgery to remove adenoma (can cause infection, hypopituitary, diabetes insipidus)

2nd line - somatostatin analogues/dopamine agonists inhibit GH secretion, GH antagonist, external radiotherapy

56
Q

Conn’s Syndrome - Causes

A

Solitary aldosterone producing adrenal adenoma 2/3

Bilateral adrenocortical hyperplasia 1/3

57
Q

Conn’s Syndrome - Pathology

A

Excess aldosterone independent of RAAS causes increased K+ loss, Na+ and water retention → raised BP, decreased renin release, hypokalaemia

58
Q

Conn’s Syndrome - Symptoms

A

Usually asymptomatic

Hypertension, increased risk of cardiac arrhythmias

Symptoms of hypokalaemia: constipation, muscle weakness, cramps,polyuria

59
Q

Conn’s Syndrome - Differential Diagnosis

A

Secondary hyperaldosteronism (excess renin which stimulates aldosterone release)

60
Q

Conn’s Syndrome - Investigations

A

U&Es - decreased renin, increased aldosterone

ECG - flat T, ST depression, long QT, long PR

61
Q

Conn’s Syndrome - Treatment

A

Laparoscopic adrenalectomy

Oral spironolactone (aldosterone antagonist)

62
Q

Addison’s Disease - Epidemiology

A

Very rare, more common in females

63
Q

Addison’s Disease - Pathology

A

Reduced cortisol level leads to increased CRH and ACTH (hyperpigmentation) production

64
Q

Addison’s Disease - Causes of adrenal insufficiency (primary and secondary)

A

Primary

  • Adrenal TB
  • Surgical removal of adrenal glands
  • Adrenal haemorrhage
  • Addison’s

Secondary

  • Steroids
  • Congenital
  • Trauma
  • CRH deficiency
  • Radiotherapy

Most common worldwide is TB, most common in the UK is Addison’s

65
Q

Addison’s Syndrome - Symptoms

A

Non specific symptoms (nausea ,abdominal pain, weight loss, anorexia, depression)

Signs - hypotension, hyperpigmentation, vitiligo, hypoglycaemia

TANED TIRED TONED TEARFUL

66
Q

Addison’s Syndrome - Investigations (3)

A
  • Short ACTH stimulation test - take baseline cortisol levels, give ACTH then measure cortisol, will remain low in Addison’s
  • Plasma ACTH levels - high ACTH with low or normal cortisol = primary hypoadrenalism. Low ACTH and cortisol = secondary or tertiary hypoadrenalism
  • U&E - shows high plasma renin due to low aldosterone and raised urea
67
Q

Addison’s Syndrome - Treatment

A
  • Glucocorticoids - oral hydrocortisone/prednisolone to replace cortisol
  • Mineralocorticoids - fludrocortisone to replace aldosterone
68
Q

Thyroid Cancer - Symptoms

A

Thyroid nodules

Dysphagia (difficulty swallowing)

Hoarse voice

Enlarged lymph nodes

69
Q

Thyroid Cancer - Investigations

A

Biopsy - to distinguish benign and malignant

Ultrasound

70
Q

Thyroid Cancer - Treatment

A

Follicular and papillary:

  • Total thyroidectomy
  • Ablative radioiodine

Anaplastic and lymphoma:

  • Radiotherapy
  • Largely palliative treatment
71
Q

SIADH - Pathology

A
  • Excess ADH → insertion of aquaporin 2 channels → water retention → dilution of blood plasma → hyponaetraemia
  • Water retention also decreases RAAS aldoseterone secreting Na+ so body is removing sodium from blood that already has low concentration
72
Q

SIADHS - Causes (5 with examples)

A

Malignancy

  • Small cell lung carcinoma
  • Prostate
  • Thymus
  • Pancreas

Drugs

  • Opiates
  • Chlorpropamide
  • Carbamazepine
  • Vincristine

Brain issues

  • Meningitis
  • Cerebral abcess
  • Head injury
  • Tumour

Lung

  • Pneumonia
  • TB
  • Abscesses
  • Asthma
  • CF

Metabolic

  • Porphyria
  • Alcohol withdrawal
73
Q

SIADHS - Symtoms (7)

A
  • Confusion
  • Irritability
  • Headaches
  • Anorexia
  • Nausea
  • Concentrated urine
  • Mild dilutional hyponatraemia
74
Q

SIADHS- Investigation

A

1-2L of 0.9% saline - sodium depletion will respond, SIADH will not

75
Q

SIADHS - Diagnostic Criteria (5)

A
  • Low serum sodium
  • Low plasma osmolality with inappropriate urine osmolarity
  • Continued urinary sodium excretion
  • Absence of hypokalaemia, hypotension and hypovolaemia (body losing fluid)
  • Normal renal, adrenal and thyroid function
76
Q

SIADHS - Treatment (4)

A
  • Restrict fluid - to increase Na+ concentration
  • Demeclocycline - inhibits action of vasopressin on kidney
  • Tolvaptan - vasopressin receptor antagonist, treats the hyponatraemia
  • Oral furosemide - salt and loop diuretics to prevent circulatory overload
77
Q

Diabetes Insipidus - Pathology (types)

A
  • Cranial - too little ADH from posterior pituitary gland
  • Nephrogenic - kidney not responding to ADH
78
Q

Diabetes Insipidus - Causes

A

Cranial:

  • Neurosurgery
  • Head trauma
  • Pituitary tumour
  • Congenital defect in ADH gene

Nephrogenic:

  • Drugs
  • Hypokalaemia
  • Hpercalcaemia
  • Sickle cell disease
79
Q

Diabetes Insipidus - Symptoms (3)

A
  • Polyuria (excess urination)
  • Polydipsia (excessive thirst)
  • Dehydration
80
Q

Diabetes Insipidus - Investigations (3)

A
  • Water deprivation test - determines whether kidneys continue to produce dilute urine despite dehydration. Restrict fluid then measure urine osmolarity. If it stays he same = Nephrogenic. Osmolarity increases = cranial
  • Plasma biochemistry
  • MRI of hypothalamus
81
Q

Diabetes Insipidus - Treatment

A

Cranial:

  • Desmopressin

Nephrogenic:

  • Bendroflumethiazide - causes more Na+ secretion in DCT → increased water loss causes GFR reduction
  • NSAIDs - reduce GFR by inhibiting prostaglandin synthase
82
Q

Hyperkalaemia - Pathology

A

Blood potassium rises → reduces difference in electrical potential between cardiac myocytes and outside → action potential threshold decreases → arrhythmias → cardiac arrest

83
Q

Hyperkalaemia - Causes (4)

A
  • Excess fluids
  • Adrenal insufficiency (aldosterone not stimulating secretion of K+ in kidneys)
  • Drugs - ACE inhibitors (block aldosterone), Spironolactone (potassium-sparing diuretic), NSAIDs
  • Acute kidney injury (decreased filtration rate)
84
Q

Hyperkalaemia - Symptoms (6)

A
  • Muscle weakness
  • Impaired neuromuscular transmission
  • Flaccid paralysis
  • Chest pain
  • Metabolic acidosis
  • Tachycardia
85
Q

Hyperkalaemia - Investigations

A
  • U&Es - over 5.5mmol/L = hyperkalaemic, over 6.5 = emergency
  • ECG - tall tented T waves, small P waves, wide QRS
86
Q

Hyperkalaemia - Treatment

A

Mild to moderate

  • Treat underlying cause
  • Dietary potassium restriction
  • Furosemide

Severe

  • Calcium gluconate - reduces excitability of cardiac myocytes
  • Insulin and dextrose - drives K+ into cells
  • Polystyrene sulphonate resin - binds K+ in gut decreasing uptake
87
Q

Hypokalaemia - Pathology

A
  • Low K+ in serum causes water concentration gradient out of cell
  • Hyperpolarisation of the myocyte membrane decreases myocyte excitability
88
Q

Hypokalaemia - Causes (4)

A
  • Anorexia
  • High aldosterone (Cushings/Conns)
  • Increased renal excretion
  • GI losses (vomiting, laxatives)
89
Q

Hypokalaemia - Symptoms (5)

A
  • Muscle weakness
  • Cramps
  • Tetany
  • Palpitations
  • Constipation
90
Q

Hypokalaemia - Investigations

A
  • U&E - <3.5mmol/L = hypokalaemia, <2.5 = emergency
  • ECG - Small/inverted T waves, depressed ST segments, long PR, long QT, prominent U waves
91
Q

Hypokalaemia - Treatment

A

Mild

  • Oral K+

Severe

  • IV K+
92
Q

Hypoparathyroidism - Causes (5)

A
  • Autoimmune destruction of parathyroid glands
  • Vit D deficiency
  • Magnesium deficiency
  • Congenital
  • Parathyroidectomy
93
Q

Hypoparathyroidism - Symptoms (mneumonic)

A

SPASMODIC

Spasms

Perioral paraesthesia (burning feeling around the mouth)

Anxious, irritable, irrational

Seizures

Muscle tone increases

Orientation impaired

Dermatitis

Impetigo herpetiformis

Chvostek’s sign (tapping over parotid gland causes twitching of ipsilateral facial muscles)

94
Q

Hypoparathyroidism - Treatment (3)

A
  • Calcium supplement
  • Calcitriol (active vit D)
  • Synthetic PTH
95
Q

Hyperparathyroidism - Causes (primary, secondary, tertiary)

A

Primary

  • Single parathyroid adenoma

Secondary

  • Compensatory hypertrophy of glands in response to hypocalcaemia

Tertiary

  • Parathyroid hyperplasia after secondary
  • Plasma calcium and PTH raised
  • Treated by parathyroidectomy
96
Q

Hyperparathyroidism - Symptoms (7)

A
  • Painful bones
  • Renal stones
  • Psychiatric moans
  • Abdominal groans
  • Thirst
  • Polyuria
  • Fractures
97
Q

Hyperparathyroidism - Investigations (3)

A
  • Bloods - primary ( inc PTH, inc Ca, dec phosphate), secondary (inc PTH, dec Ca, inc phosphate) tertiary (inc everything)
  • Abdominal X-ray - renal calculi or nephrocalcinosis
  • Radioisotope scanning - adenomas
98
Q

Hyperparathyroidism - Treatments (primary, secondary, tertiary)

A

Primary

  • Parathyroid adenoma - surgical removal
  • Parathyroid hyperplasia - all 4 glands removed
  • Calcimimetic - increases sensitivity to Ca2+ → less PTH secretions

Secondary and tertiary

  • Treat cause

Emergency

  • Rehydrate
  • Bisphosphonates (inhibits osteoclasts → prevents bone resorption)
99
Q

Pseudohypoparathyroidism - Description, Investigation, Treatment

A

Resistance to PTH due to genetic mutation

Bloods show low calcium and high PTH

Treat as normal hypoparathyroidism

100
Q

Hypocalcaemia - Causes (7)

A
  • Vit D deficiency - low phosphate, low calcium uptake in GI and decreased absorption in kidneys leads to osteomalacia
  • Hypoparathyroidism - high phosphate
  • Acute pancreatitis - high phosphate
  • Osteomalacia - low phosphate, soft bones due to low calcium and vit D deficiency
  • Chronic Kidney Disease - high phosphate, poor uptake of calcium in kidneys caused by low production of vit D
  • Pseudohypoparathyroidism - resistance to PTH
  • Drugs - calcitonin (decreases calcium and phosphate), bisphosphonates (reduce osteoclast activity)
101
Q

Hypocalcaemia - Symptoms (mnemonic)

A

SPASMODIC

Spasms

Perioral paraesthesia (burning feeling around the mouth)

Anxious, irritable, irrational

Seizures

Muscle tone increases

Orientation impaired

Dermatitis

Impetigo herpetiformis

Chvostek’s sign (tapping over parotid gland causes twitching of ipsilateral facial muscles)

102
Q

Hypocalcaemia - Investigations

A

ECG - long QT interval

103
Q

Hypocalcaemia - Treatments

A

Mild - adcal supplement (calcium corbonate)

Severe - Calcium gluconate

104
Q

Hypercalcaemia - Epidemiology

A

Mostly affects older women

105
Q

Hypercalcaemia - Causes

A

Most common is hyperparathyroidism or cancer

CHIMPANZEES

Calcium supplementation

Hyperparathyroidism

Iatrogenic drugs

Milk alkali syndrome

Paget’s disease of bone

Acromegaly and Addison’s

Zolinger-Ellison Syndrome

Excess vit D

Excess vit A

Sarcoidosis

106
Q

Hypercalcaemia - Symptoms (5)

A
  • Painful bones - osteitis fibrosa cystica
  • Renal stones - calcium deposition in renal tubules causes polyuria and nocturia
  • Psychiatric moans - lethargy, fatigue, memory loos, psychosis, depression
  • Abdominal groans - nausea, vomiting, constipation, indigestion
  • Cardiac arrest
107
Q

Hypercalcaemia - Investigations

A
  • ECG - tented T, short QT interval
  • Bloods - undetectable PTH excludes primary hyperparathyroidism (check for tumour)
108
Q

Hypercalcaemia - Treatments

A
  • Treat underlying cause
  • IV saline - dilutes calcium
  • Bisphosphonates - encourage osteoclasts to undergo apoptosis so less breakdown
109
Q

Hyperprolactinaemia - Epidemiology

A

Common in young women

110
Q

Hyperprolactinaemia - Causes

A

Prolactin secreting pituitary adenoma (prolactinoma)

Any tumour inhibiting dopamine (as this inhibits prolactin)

111
Q

Hyperprolactinaemia - Symptoms (4)

A
  • Increased prolactin → increased milk production
  • Reduced fertility (prolactin inhibits GnRH)
  • Decreased libido, erectile dysfunction
  • Amenorrhoea
112
Q

Hyperprolactinaemia - Investigations (3)

A
  • Serum prolactin level
  • Thyroid function tests
  • MRI of pituitary
113
Q

Hyperprolactinaemia - Treatment

A

Dopamine agonist - Cabergoline or Bromocriptine

Phase 2a (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions