Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a Stuff > Endocrinology and Diabetes > Flashcards

Endocrinology and Diabetes Flashcards

1
Q

Define T1DM

A

Metabolic autoimmune disorder from destruction of insulin producing beta cells in the pancreas, resulting in absolute insulin deficiency.

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

Causes of T1DM

A

HLA-DR and HLA-DQ provide protection from or increase susceptibility to diabetes. Environmental factors and viruses may trigger the destruction of beta cells.

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

T1DM risk factors

A

Western countries, FHx, infectious agents, dietary factors.

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

Key presentations of T1DM

A

Polyuria, polydipsia, blurred vision, fatigue, weight loss

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

Signs that a patient has T1DM and not T2DM.

A

Weight loss, young age, FHx of autoimmune disease

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

1st Line investigation for DM

A

Random glucose tolerance test >11.1mmol/L

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

Gold standard investigation for DM

A

HbA1c testing >6.5%

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

Other tests for DM

A

Fasting plasma glucose, 2-hour plasma glucose, plasma/urinary ketones. Low C peptide levels.

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

Criteria for diagnosing diabetes mellitus using glucose testing.

A

Symptoms plus:

  • random glucose >11.1
  • fasting glucose >7
  • 2hr glucose >11.1 after oral GTT

With NO symptoms need 2 confirmatory tests

Ranges are lower when testing for gestational diabetes

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

Differential diagnosis for T1DM

A

T2DM, other types of diabetes

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

Management of T1DM

A

Basal-bolus insulin
Pre-meal insulin correction dose
Amylin analogue
2nd line is fixed insulin dose

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

Microvascular complications of DM

A

Retinopathy, nephropathy, neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Macrovascular complications of DM

A

CAD, cerebrovascular disease, peripheral artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of untreated DM

A

Hyperosmolar hyperglycaemic state, DKA, blindness, renal failure, foot amputations, MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Complication of overtreating DM

A

Hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathogenesis of T1DM

A
  • Autoimmune pancreatic beta-cell destruction
  • Up to 90% have autoantibodies to glutamic acid decarboxylase, insulin or islet auto-antigen 2
  • Cell destruction proceeds sub-clinically for a long time as insulitis before developing hyperglycaemia after 80-90% cell loss.
  • Pts cannot use glucose in peripheral muscles stimulating glucagon secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define T2DM

A

Insulin resistance (and less severe insulin deficiency) due to prolonged nutrient excess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Potential causes of T2DM

A

Genetic factors affecting beta-cell development
Beta-cell function with age
Not really any concrete reasons people develop T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Risk factors of T2DM

A

Males, certain ethnicities, elderly, central obesity, lack of exercise, high calorie intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Key presentations for T2DM

A

Polyuria, polydipsia, fatigue, blurred vision, genital thrush, hunger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophysiology of T2DM

A
  • Impaired ability of insulin which increases plasma glucose
  • As insulin resistance develops the body shows hypersecretion of insulin before it lowers
  • Glucagon and other counterregulatory hormones are secreted more
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why is the insulin response to oral glucose different to that of IV glucose?

A

GLP-1 and GIP are incretins released in the GI tract after eating, increasing insulin response. Both of these have short half lives and are broken down by DPP4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What effects does T2DM have on the nephron (not complications)?

A

Upregulates reabsorption of glucose via SGLT2 channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Management of T2DM (in order)

A 
Lifestyle Modification
METFORMIN - 1st line
2nd line - Metformin with:
- DPP4 inhibitor OR
- Pioglitazone OR
- Sulphonylurea OR
- SGLT2 inhibitor

Then insulin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define hypoglycaemia

A

A low blood glucose level. <3.0mmol/L represents severe hypoglycaemia and below 4 is an ‘alert level’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hypoglycaemia causes

A

Inappropriate doses of diabetes medication
Excessive alcohol
Skipping/Delaying meals
Intense exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hypoglycaemia risk factors

A

Elderly, males, people outside the home, longer duration of diabetes, patients only using SU.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Key presentations of hypoglycaemia

A

Blurred vision, seizures, collapsing, confusion, unusual behaviour, fatigue, feeling hungry
Waking after sleep with headaches, tiredness or night sweats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hypoglycaemia management

A

Glucose (oral or IV)

Glucagon and adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

DKA management

A

Fluids and insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

DKA features

A

acidaemia, hyperglycaemia, ketonemia/ketonuria

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

Difference between DKA and HHS

A

HHS shows no features of ketogenesis

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

HHS treatment

A

Fluids and anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Define hyperthyroidism

A

Elevated levels of T4/T3 in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Causes of hyperthyroidism

A

75-80% of all cases are caused by Graves’ disease
Toxic multinodular goitre
Toxic adenoma
Other rare causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Hyperthyroidism risk factors

A

Female, elderly, recent pregnancy, autoimmune disease (or FHx), thyroid problems or surgery.

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

Pathophysiology of hyperthyroidism

A

Overproduction of thyroid hormones OR;
Leakage of preformed thyroid hormones OR;
Ingestion of excess thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Key presentations of hyperthyroidism

A

Heat intolerance, tachycardia, weight loss, oligomenorrhoea, goitre, HTN, proximal muscle wasting, thirst, sweating

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

1st line investigations for hyperthyroidism

A

TFTs (TSH and T3/4 levels)
Thyroid antibody tests (for Graves’ disease)
- TPO
- Thyroglobulin antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

The gold standard test for hyperthyroidism

A

TFTs

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

Other testing for hyperthyroidism

A

Radioactive iodine isotope uptake scan (if antibody negative)

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

Differential diagnosis of hyperthyroidism

A

Thyroid ultrasound differentiates Graves’ from toxic adenoma

- TSHRAb testing

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

Hyperthyroidism management

A 
Anti-thyroid drugs (carbimazole)
- Titration or block and dose regimen
Radioiodine 131 Iodine
Surgery if other options don't work or previously rendered euthyroid
Beta blockers (against HTN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Complications of Hyperthyroidism

A

Heart issues, eye problems, skin issues, osteoporosis

THYROID STORM

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

What happens in a thyroid storm?

A

Untreated hyperthyroidism causes very high BP, HR and temperature

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

Define hypothyroidism

A

Abnormally low levels of T3/4 in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Gender differences in hypothyroidism

A

Much more common in women than men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hypothyroidism causes

A

Primary

  • Primary atrophic hypothyroidism
  • Hashimoto’s thyroiditis
  • Postpartum thyroiditis, iodine deficiency, hyperthyroidism therapy

Secondary and tertiary
- Pituitary/Hypothalamic dysfunction

Certain drugs (lithium, amiodarone, interferon-a)
T3 resistance
Isolated TSH deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Hypothyroidism risk factors

A

Female, FHx, elderly, autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Key presentations of hypothyroidism

A

Fatigue, cold intolerance, bradycardia, dry skin and hair, mental slowness, pallor, weight gain (myxoedma), goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

1st line tests for hypothyroidism

A

TFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Gold Standard test for hypothyroidism

A

TFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Other tests for hypothyroidism

A

Anaemia testing
Increased cholesterol and triglyceride levels
Hyponatraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Differential diagnosis of hypothyroidism

A

T1DM, Addison’s, Coeliac or other autoimmune conditions
Anaemia and multiple myeloma
End organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Management of hypothyroidism

A 
ORAL LEVOTHYROXINE (lifelong replacement of T4)
Surgery if needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Hypothyroidism complications

A

Myxoedema coma
Myxoedema ‘madness’
Hyperthyroidism from over-treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Myxoedema coma treatment

A 
Oral T3
Oxygen
Monitor CO and BP
Gradual rewarming
Hydrocortisone
Glucose infusion to prevent hypoglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Define Graves’ disease

A

Autoimmune process that is the most common cause of hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Graves’ disease pathophysiology

A

Serum IgG antibodies bind to TSH receptors in the thyroid, stimulating thyroid hormone production. TSH receptor antibodies are specific for Graves’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Clinical manifestations of Graves’ disease

A

Hyperthyroidism presentations

Graves’ ophthalmology (bulging eyes, increased tears, photophobia, diplopia, extraocular muscle swelling)

Graves’ dermopathy (pretibial myxoedema)

Thyroid acropathy (clubbing and swollen fingers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

1st line and gold standard investigation for Grave’s disease

A

TSHR-Ab levels raised (TSH testing already done to establish hyperthyroidism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Management of Grave’s disease

A

Hyperthyroidism management

Corticosteroids for ophthalmopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Grave’s disease complications

A

Pregnancy issues, heart disorders, thyroid storm, osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Define Hashimoto’s thyroiditis

A

Autoimmune disease causing thyroid gland damage and primary hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Triggers of Hashimoto’s thyroiditis

A

Iodine, infection, smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Hashimoto’s thyroiditis pathophysiology

A

Cytotoxic (CD8+) cell-mediated thyroid destruction. Patients are hypothyroid but go through an initial toxic phase (Hashi-toxicity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Investigations for Hashimoto’s thyroiditis

A

TFTs, TPO-Ab testing to confirm Hashimoto’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Management for Hashimoto’s

A

Levothyroxine therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Complications of Hashimoto’s

A

Heart problems
Myxoedema coma
Mental health issues
Hypothyroid complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Define Cushing’s syndrome

A

Increased plasma glucocorticoids (cortisol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Causes of Cushing’s syndrome

A

Increased ACTH from pituitary tumour (CUSHING’S DISEASE)
Ectopic ACTH-producing tumours
Increased cortisol due to adrenal adenoma or carcinoma
Exogenous steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Key presentations of Cushing’s syndrome

A

Central obesity, thin skin, acne, proximal muscle wastage.

Moon face, buffalo hump, striae, mental changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

1st line tests for Cushing’s syndrome

A

48hr low-dose dexamethasone test (Cushing’s fail to suppress cortisol)
24hr urinary free cortisol
Loss of cortisol circadian rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Gold standard test for Cushing’s syndrome

A

Inferior petrosal sinus sampling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

2nd line tests for Cushing’s syndrome

A

ACTH plasma levels, adrenal MRI/CT, pituitary MRI, CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Cushing’s syndrome management

A

Cortisol hypersecretion should be controlled prior to surgery (metyrapone)

Trans-sphenoidal removal of tumour (Cushing’s disease)

Other causes often also require surgically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Prognosis of Cushing’s syndrome

A

Very poor if untreated, adrenal carcinomas also have poor prognosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Define Acromegaly

A

Excessive GH after fusion of the epiphyseal plates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Define Gigantism

A

Excessive GH before fusion of the epiphyseal plates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Acromegaly causes

A

GH-secreting pituitary tumour (most common), ectopic GHRH excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What does increased GH cause?

A

Increased IGF-1 levels leading to the changes seen in acromegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Key presentations of acromegaly.

A

Thicker skin, increased hand and foot size, facial changes, visual disturbances, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

1st line test for acromegaly

A

GH levels (to rule out acromegaly as detectable levels aren’t diagnostic)

84
Q

Gold standard test for acromegaly

A

Glucose tolerance test (diagnostic if there is no suppression of GH)

85
Q

Other tests for acromegaly

A

Visual field exam, MRI scan, pituitary function test, prolactin level (for co-secreting tumours)

86
Q

1st line management for acromegaly

A

Trans-sphenoidal surgery

87
Q

Drug management for acromegaly

A

Pituitary radiotherapy
SMS agonists - Octreotide
DA agonists
GH antagonists - Pegvisomant

88
Q

Complications of acromegaly

A

HTN, enlargement of heart, osteoarthritis, T2DM, goitre, vision loss etc.

89
Q

Causes of primary hyperaldosteronism

A

Adrenal adenoma secreting aldosterone (CONN’S SYNDROME)

Bilateral adrenocortical hyperplasia

90
Q

Risk factors for primary hyperaldosteronism

A

Hypertension

91
Q

Pathophysiology of primary hyperaldosteronism

A

Aldosterone causes increased exchange of Na+ and K+ in the DCT as well as increased water retention.

This causes hypokalaemia and increased BP.

92
Q

1st line investigations for primary hyperaldosteronism

A 
Discontinue drugs that can affect renin activity
Plasma aldosterone : renin ratio (ARR)
Serum hypokalaemia (not always present)
Bilateral adrenal vein sampling
93
Q

Other investigations for primary hyperaldosteronism

A

High urinary K+, ECG, CT/MRI adrenals

94
Q

Differential diagnosis of primary aldosteronism

A

Secondary hyperaldosteronism (from high renin and angiotensin II levels)

Different hyperplasia from Conn’s disease with adrenal CT/MRI

95
Q

Management of primary hyperaldosteronism

A

Laparoscopic surgery. Aldosterone antagonists - Spironolactone

96
Q

Complications of primary hyperaldosteronism

A

Heart attacks, heart failure, kidney failure, early death

97
Q

Causes of pituitary mass lesions

A

Non-functioning pituitary adenomas, craniopharyngioma, Rathke’s cysts, meningioma, lymphocytic hypophysitis

98
Q

Local effects of pituitary mass lesions

A

Bilateral hemianopia, headache, hypopituitarism, cranial nerve palsy

99
Q

Gold standard test for pituitary mass lesion

A

MRI pituitary

100
Q

Other tests in pituitary mass lesions

A

Hormone tests, visual defect test

101
Q

Treatment of choice for pituitary mass lesions

A

Trans-sphenoidal surgery.

Then radiotherapy with SMS and DA agonists. Treatment for any hormone imbalances.

102
Q

Define Addison’s disease (primary adrenal insufficiency)

A

Destruction of the entire adrenal cortex. This results in aldosterone, cortisol and androgen deficiency.

103
Q

Causes of Addison’s disease

A

Autoimmune adrenalitis
TB
Surgical removal of adrenal cortex
Schilder’s disease

104
Q

Key presentation of Addison’s disease

A

Postural hypertension, bronze pigmentation of skin, weight loss and wasting, confusion, GI disturbance, polydipsia

105
Q

1st line investigations for Addison’s disease

A

Synacthen test (short ACTH stimulation test)

Adrenal antibodies
Bloods - cortisol, raised calcium and potassium, low sodium
Hypoglycaemia

106
Q

Gold standard test Addison’s disease

A

Synacthen test

means syn. ACTH en test!

107
Q

Other investigations used in Addison’s disease diagnosis

A

CXR, AXR

108
Q

Differential diagnosis

A

Secondary adrenal insufficiency - no bronze pigmentation, stop causative drugs

109
Q

Addison’s disease management

A

Hydrocortisone
Fludrocortisone (replaces aldosterone)
Mineralocorticoids to correct postural hypotension

110
Q

Complication of Addison’s disease

A

ADRENAL CRISIS

111
Q

Describe an adrenal crisis

A

Hypotension and CV collapse - SHOCK
Hyponatraemia, hyperkalaemia

Treatment: Fluids and IV hydrocortisone ASAP

112
Q

Define hyperkalaemia

A

Inappropriately high blood potassium level >5.0mmol/L

113
Q

Causes of hyperkalaemia

A 
Vigorous exercise (self-limiting)
Low levels of aldosterone
Kidney disease
Excessive consumption (IV fluids)
Increased cellular release in acidosis
Drugs (beta blockers)
114
Q

Risk factors for hyperkalaemia

A

CKD

Diabetes (DKA)

115
Q

Pathophysiology of hyperkalaemia

A

Insulin deficiency = not enough K+ follows insulin into cells

Acidosis = H+ exchanged into cells with K+

Beta blockers inhibit K+ pumping into cell

Cell lysis causes intracellular K+ to be released

116
Q

Key presentations of hyperkalaemia

A

Cramping, weakness/flaccid paralysis, arrhythmias and arrest

Kussmaul respiration (if metabolic acidosis)

117
Q

1st line tests for hyperkalaemia

A

U+Es, urinary K+

118
Q

Other tests for hyperkalaemia

A

ECG, creatinine, GFR evaluation

119
Q

Urgent management of hyperkalaemia

A

Insulin

Calcium gluconate

120
Q

Non-urgent management of hyperkalaemia

A

Potassium binders (decrease uptake in gut)

121
Q

ECG for hyperkalaemia

A

Tall, tented T waves, small P waves and wide QRS complexes

122
Q

Define hypokalaemia

A

Inappropriately low blood potassium (<3.5mmol/L)

123
Q

Causes of hypokalaemia

A 
DIURETIC TREATMENT
Hyperaldosteronism
Beta-2 agonists
Renal disease (Gitelman's, Liddle's Bartter's)
Vomiting/Diarrhoea
Too much insulin
Alkalosis
124
Q

Pathophysiology of hypokalaemia

A

K+ uptake into cells is stimulated by insulin, beta-adrenergic stimulation and theophyllines.

Potassium levels are also heavily controlled by the kidneys (90% of filtered K+ is reabsorbed in PCT) and potassium is also secreted from the principal cells of the collecting ducts.

Aldosterone stimulates K+ and H+ secretion in exchange for Na+ in the principal cells – decreased K+ stimulates aldosterone.

125
Q

Key presentations of hypokalaemia

A

Usually asymptomatic
Arrhythmias and palpitations
Cramps, muscle weakness, constipation

126
Q

1st line test for hypokalaemia

A

U+Es, urinary K+

127
Q

Other tests for hypokalaemia

A

ABG to test alkalosis
Digoxin tests
TSH tests
ECG

128
Q

Management of hypokalaemia

A

Mild - oral K+
Severe - IV K+
Aldosterone receptor antagonists if hyperaldosteronism

129
Q

Complications of hypokalaemia

A

Bradycardia with CV collapse, arrhythmias and acute respiratory failure from muscle paralysis.

130
Q

ECG changes in hypokalaemia

A

U wave present, no t wave/t wave inversion, long PR and long QT

131
Q

Define SIADH

A

Inappropriately high secretion of ADH which leads to increased water retention and hyponatraemia.

Characterised by euvolaemia.

132
Q

Causes of SIADH

A

Ectopic ADH production (lung cancer or infections)

CNS causes

Drugs (CARDISH)

  • Chemotherapy
  • Antidepressants
  • Recreational drugs
  • Diuretics
  • Inhibitors (ACEi or SSRIs)
  • Sulphonylureas
  • Hormones
133
Q

Pathophysiology of SIADH

A

Increased ADH = increased water reabsorption. This increases blood volume and decreases plasma osmolality, therefore causing dilutional hyponatraemia.

Increased blood volume causes the heart to release ANP and BNP which decreases blood volume back to normal and even further decreases plasma osmolality.

Causes euvolaemia, hyponatraemia and high urinary sodium.

134
Q

Key symptoms of SIADH

A

Headache, nausea, mental slowing, confusion, unstable gait.

Acute symptoms include coma, convulsion and respiratory arrest.

135
Q

1st line investigations for SIADH

A

Plasma (<275) and urine osmolality (>100). Spot urine sodium (>40)

136
Q

Other investigations for SIADH

A

TSH, cortisol, assessment of underlying causes (CXR)

137
Q

Management of SIADH

A

Remove causal factor

Fluid restriction <1L/24hr if asymptomatic. Sometimes you need demeclocycline if fluid restriction if not tolerated.

Severe symptomatic cases require hypertonic saline.

138
Q

Definition of DI

A

Insufficient amount of ADH

139
Q

Causes of DI

A

Cranial DI = posterior pituitary producing too little ADH

Nephrogenic DI = kidney does not respond to the ADH in the blood

140
Q

Key presentations of DI

A

Polyuria, polydipsia and dehydration

141
Q

1st line investigation for DI

A

Water deprivation test

Hypertonic saline test - measures copeptin levels

142
Q

Management of DI

A

Cranial DI = desmopressin

Nephrogenic DI = Bendroflumethiazide, NSAIDs - more difficult to treat

Excision of tumour if indicated

143
Q

Complications of DI

A

Chronic dehydration, hypotension, kidney damage, tachycardia, weight loss

144
Q

Define hypercalcaemia

A

An excess of calcium in the blood >2.6mmol/L

145
Q

Causes of hypercalcaemia

A

Hypercalcaemia of malignancy
Primary hyperparathyroidism
Drugs - thiazides, vitamin D analogues, vitamin A, lithium
Excessive calcium intake (milk-alkali syndrome)

146
Q

Risk factors for hypercalcaemia

A

Immobility, FHx, severe dehydration, drug use

147
Q

Pathophysiology of hypercalcaemia

A

PTH increases calcium reabsorption, vitamin D activation in the kidney and increases bone resorption

In primary hyperparathyroidism is when there is an inappropriate rise in PTH despite a rise in calcium.

148
Q

Key presentations of hypercalcaemia

A 
Bones - pain, osteoporosis
Stones - kidney stones
Moans - abdominal pain, constipation
Groans - confusion, anxiety
Seizure - short QT interval
149
Q

1st line investigations for hypercalcaemia

A

Raised serum calcium
24hr urinary calcium
PTH levels

150
Q

Other investigations for hypercalcaemia

A

Renal function baseline
Malignancy investigation
Serum TSH and ACTH

151
Q

Differential diagnosis of hypercalcaemia

A

Albumin levels

152
Q

Management of hypercalcaemia

A

Aggressive rehydration - IV 0.9% saline
Bisphosphonates (IV pamidronate)
Oral prednisolone

Long-term you control the underlying malignancy (chemo or radio)

Parathyroid surgery if primary hyperparathyroidism

153
Q

Define hypocalcaemia

A

Low levels of calcium in the blood (<2.1mmol/L)

154
Q

Causes of hypocalcaemia

A

Vitamin D deficiency
Hypoparathyroidism
Pseudo-hypoparathyroidism (PTH resistance)
Increased phosphate levels due to CKD or phosphate therapy

155
Q

Pathophysiology of hypocalcaemia

A

Low levels of PTH or a resistance to PTH causes decreased calcium reabsorption and decreased bone resorption

Low vitamin D levels decreases gut absorption of calcium

156
Q

Key presentations of hypocalcaemia

A 
Chvostek's sign
Trousseau's sign
Numbness, cramps, anxiety, neuromuscular issues
Cataracts, prolonged QT on ECG. 
Muscle spasms and seizures
157
Q

1st line test for hypocalcaemia

A

Serum calcium
PTH levels
Serum and urine creatinine

158
Q

Other tests for hypocalcaemia

A

25-hydroxyvitamin D level, parathyroid antibodies, magnesium levels, metacarpal x-ray

159
Q

Differential diagnosis of hypocalcaemia

A

GI tract dysfunction

Low albumin levels

160
Q

Management of hypocalcaemia

A

In vitamin D deficiency use cholecalciferol

In other cases, alpha-hydroxylated vitamin D derivatives

Oral calcium supplements

Severe symptoms require calcium gluconate

161
Q

Complications of hypocalcaemia

A

Acute seizures/tetany, basal ganglia calcification, parkinsonism

162
Q

Causes of hyperparathyroidism

A

Primary - parathyroid adenoma, hyperplasia, carcinoma, lithium (results in hypercalcaemia)

Secondary - vitamin D resistance (results in hypocalcaemia)

Tertiary - glands become autonomous after many years of secondary hyperparathyroidism (results in hypercalcaemia)

163
Q

Key presentations of hyperparathyroidism

A

Primary - often asymptomatic

Secondary - kidney disease with skeletal or CV complications

164
Q

1st line testing for hyperparathyroidism

A

Serum calcium and PTH, raised alkaline phosphatase

165
Q

Gold standard testing for hyperparathyroidism

A

PTH immunoassay

166
Q

Other tests for hyperparathyroidism

A

Ultrasound, radioisotope scans, DEXA bone density scan

167
Q

Management of hyperparathyroidism

A

Treat severe hypercalcaemia first – medical emergency
Primary – surgical removal of adenoma
Secondary and tertiary – calcium correction - calcimimetics
Total or subtotal parathyroidectomy
Bisphosphonates
Chemotherapy in malignancy

168
Q

Hyperparathyroidism complications

A

Kidney stones, acute pancreatitis, peptic ulceration, calcification of the cornea

169
Q

Causes of hypoparathyroidism

A

Genetic diseases - Di George syndrome

Acquired - complication of surgery or radiotherapy

Transient - premature neonates

Inherited - pseudohypoparathyroidism, pseudopseudohypoparathyroidism

170
Q

Risk factors for hypoparathyroidism

A

Recent neck surgery, FHx

171
Q

1st line tests for hypoparathyroidism

A

PTH level, serum calcium and phosphate, 24hr urine calcium, creatinine

172
Q

Gold standard testing for hypoparathyroidism

A

Parathyroid immunoassay

173
Q

Other tests used in hypoparathyroidism

A

Hand x-ray, ECG, ECHO of heart (Di George)

174
Q

Management of hypoparathyroidism

A

Diet high in calcium and low in phosphates

Calcium and vitamin D supplements

175
Q

Complications of hypoparathyroidism

A

Kidney stones, arrhythmias, cataracts, dental and bone disorders

176
Q

Causes of neuroendocrine tumours

A

MEN1 or MEN2
Neurofibromatosis type 1
VHL syndrome
ALL ARE INHERITED CONDITIONS

177
Q

Key presentations for neuroendocrine tumours

A

Depends on where in the body it is.

GI - diarrhoea, constipation, abdomen pain

Lung - wheezing and cough

Symptoms caused by increased hormone levels

178
Q

Prognosis of neuroendocrine tumours

A

Poor prognosis since most tumours are diagnosed after having spread

179
Q

Define pheochromocytoma

A

Rare tumour of the adrenal medulla that secretes adrenaline and noradrenaline.

A tumour of the sympathetic NS

180
Q

Risk factors of pheochromocytoma

A

FHx of pheochromocytoma, MEN 2, VHL syndrome

181
Q

Key presentations of pheochromocytoma

A

Episodic headache, sweating, tachycardia, HTN, anxiety, GI disturbance, fever, Raynaud’s phenomenon

182
Q

1st line treatment for pheochromocytoma

A

Urinary and plasma metanephrines

Genetic testing

183
Q

Differential diagnosis of pheochromocytoma

A

Alcohol withdrawal, labile essential hypertension, hyperventilation

184
Q

Management of pheochromocytoma

A

Surgery if possible

Complete alpha and beta blockade (alpha MUST precede beta)
Iv hydration
Clinical and biochemical review

185
Q

Complications of pheochromocytoma

A

Cardiomyopathy, myocarditis, cerebral haemorrhage, PE

186
Q

Hyperprolactinaemia causes

A

Physiological

  • pregnancy
  • stress
  • sleep
  • exercise
  • sex

Pathological

  • PROLACTINOMAS
  • co-secretion in tumours causing acromegaly
  • stalk compression
  • primary hypothyroidism

Drugs

  • oestrogens
  • DA agonists
  • antidepressants
  • antiemetics
187
Q

Pathophysiology of Hyperprolactinaemia

A

Increased prolactin causes increased lactation and blocks action of GnRH and LH

188
Q

Key presentations of hyperprolactinaemia

A 
Galactorrhoea
Amenorrhoea or Oligomenorrhoea
Delayed or arrested puberty
Decreased libido
Visual defects and headache
189
Q

1st line tests for hyperprolactinaemia

A

Prolactin levels in blood (0900h to 1600h)

Pregnancy testing

190
Q

Other investigations for hyperprolactinaemia

A

Visual field defects
Anterior pituitary function tests
TFTs
Pituitary MRI

191
Q

Management of hyperprolactinaemia

A

DOPAMINE AGONISTS - Cabergoline

Trans-sphenoidal surgery rarely used if DA agonists don’t work

192
Q

Define delayed puberty

A

Absence of secondary sexual characteristics by 14 (girls) or 16 (boys). MUCH MORE COMMON IN BOYS - so with girls likely to be more serious

193
Q

Causes of delayed puberty

A

Idiopathic

Hypogonadotropic hypogonadism
- sexual infantilism related to gonadotropin deficiency

Hypergonadotropic hypogonadism
- primary gonadal issues

Constitutional delay of growth and puberty (CDGP) - just naturally late bloomers

Genetic conditions

  • Kallman
  • Klinefelter
  • Turner
194
Q

Key presentations of delayed puberty

A

Lack of secondary sex characteristics by appropriate age (Thelarche, adrenarche, pubarche, voice changes)

195
Q

1st line investigations of delayed puberty

A

Assessment of LH, FSH, oestradiol and testosterone

196
Q

Other investigations of delayed puberty

A

TFTs, bone age x-rays, assessment for pelvic abnormalities

197
Q

Management of delayed puberty

A

Sometimes non needed.

Short-term, low-dose sex hormone therapy used to induce puberty if delay is great or child’s mental health is suffering

In hypogonadism, pubertal induction is required (oestrogen then progesterone or testosterone)

198
Q

Complications of delayed puberty

A

Infertility

Mental health issues

199
Q

Define precocious puberty

A

Onset of secondary sexual characteristics before 8 (girls) or 9 (boys)

MUCH MORE COMMON IN GIRLS - with boys more likely to be serious

200
Q

Causes of precocious puberty

A 
Idiopathic
Cerebral - tumour or brain damage
CAH, McCune-Albright syndrome
Testicular or ovarian syndromes
HCG-, androgen- or oestrogen-secreting tumours (peripheral)
201
Q

Key presentations of precocious puberty

A

Early breast growth and menarche

Axial, pubic and/or facial hair.

Rapid growth, acne and body odour

202
Q

Investigations for precocious puberty

A

LH, FSH, oestrogen and progesterone or testosterone. X-ray for bone age.

203
Q

Management of precocious puberty

A

Long-acting GnRH analogues (if gonadotropin-dependent)

Inhibitors of steroidogenesis, antiandrogens and aromatase inhibitors (if gonadotropin-independent)

204
Q

Define hypopituitarism

A

Deficiency of any hormone produced in the pituitary. Panhypopituitarism = deficiency is all hormones excreted by the anterior pituitary.

205
Q

Causes of hypopituitarism

A

PROP1 and POU1F1 mutations affecting anterior development
Trauma from surgery
Pituitary or hypothalamic tumours

206
Q

Tests for hypopituitarism

A

Testing each pituitary axis
MRI pituitary
insulin tolerance test (ACTH and GH deficiency)

207
Q

Management of hypopituitarism

A

Hydrocortisone and levothyroxine ASAP

Sex hormone replacement
GH replacement
Surgery for tumours?

Phase 2a Stuff (7 decks)

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