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Phase 2a medicine > Endo > Flashcards

Endo Flashcards

1
Q

What is Type 1 diabetes?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulim deficiency

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2
Q

At what age do symptoms occur for type 1 DM?

A

5-15

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3
Q

What are the risk factors for DM1?

A

Norther European, family history HLA DR3-DQ2

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4
Q

What other autoimmune disease put you at risk of DM1?

A

Autoimmune thyroid, coeliac, addisons, pernicious anaemia

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5
Q

What does insulin deficiency lead to?

A

Breakdown of liver glycogen, hyperglyacaemuia and glycosuria

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6
Q

What are the symptoms of DM1?

A

Polydipsia, polyuria, weight loss

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7
Q

How long do symptoms for DM1 last before diagnosis?

A

A short history of severe symptoms

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8
Q

The typical patient with DM1 diagnosis?

A

S&S above, young, BMI under 25, personal/fhx autoimmune, random plasma glucose >11mmol/l

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9
Q

How to treat DM1?

A

Insulin. twice daily regime or insulin before meals and a baseline insulin

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10
Q

What is diabetic ketoacidosis?

A

Lack of insulin leading to unrestrained increased hepatic gluconeogenesis, and hyperglycaemia

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11
Q

How are ketones formed in ketoacidosis?

A

Without insulin fat is broken down, this increases fatty acids which are oxised to acetyl coa then ketones

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12
Q

What are the symptoms of diabetic ketoacidosis?

A

N&V, weight loss, drowsy, confused, abdo pain, diabetes symptoms

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13
Q

What are the signs of diabetic ketoacidosis?

A

Reduced tissue turgor, kussmauls breathing, breath smell of ketones, hypotension and tachycardia

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14
Q

What investigations for ketoacidosis?

A

Random plasma glucose >11mmol/l, plasma ketones,, acidosis in low blood pH, glycosuria and ketonuria

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15
Q

How to manage diabetic ketoacidosis?

A

ABC

fluid resuscitation, IV insulin, resotre electrolytes K+

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16
Q

What are the complications of diabetic ketacidosis?

A

Coma, cerebral oedema, thromboembolism, aspiration pneumonia, death

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17
Q

What is DM2?

A

Combination of peripheral insulin resistance and less severe insulin deficiency.

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18
Q

Risk factors for DM2?

A

Age, men, afrocarribean, black african and south asian, obesity and hypertension

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19
Q

What is the presentation of DM2?

A

Polydipsia, polyuria, glycosuria, central obesity, slower onset

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20
Q

What is the HbA1c of someone with diabetes?

A

> 47mmol/mol

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21
Q

Lifestyle management for DM2?

A

Diet, weight control, exercise

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22
Q

1st line pharmacological for DM2

A

Metformin

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23
Q

Drugs you can give alongside metformin for DM2?

A

DPP4 inhibitor, Pioglitiazone, sulfonylureas, SGLT-2i

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24
Q

How does metformin work?

A

Decreased gluconeogenesis in the liver and increased cell sensitivity to insulin

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25
Q

How do sulfonureas work?

A

Promote insulin secresion

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26
Q

What are the side effects of sulfonylureas?

A

hypoglycaemia and weight gain

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27
Q

Which patients struggle with hyperosmolar hyperglycaemic state?

A

DM2

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28
Q

How to diagnose hyperosmolar hyperglacaeimc state?

A

Hyperglycaemia >11mmol/l
Heavy glycosuria
High plasma osmolality

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29
Q

What is the treatment for hyperosmolar hyperglycaemic state?

A

Fluid replacement with saline, LMWH to decrease risk of thromboembolism
restore electrolyte loss

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30
Q

What is cushings syndrome?

A

Chronic excess of cortisol hormone released by the adrenal glands

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31
Q

Which hormone stimulates ACTH release from the anterior pituitary?

A

Corticotropin releasing hormone

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32
Q

Which part of the adrenal cortex is cortisol released from?

A

Zona fasiculata

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33
Q

What is cushings disease?

A

Caused by an ACTH secreting pituitary adenoma

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34
Q

What are ACTH independant causes of cushings?

A

Adrenal adenoma, iatrogenic

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35
Q

Presentation of patients with cushings?

A

Central obestiy, moon face, mood change, proximal muscle weakness, purple abdominal striae, gastric ulcers, osteoporosis,

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36
Q

What drugs might cause cushings?

A

Oral steroids

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37
Q

First line test for cushings

A

Random plasma cortisol, if high do more tests

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38
Q

Gold standard test for cushings?

A

Overnight dexamethasone suppression test

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39
Q

What does the dexamethasone test do?

A

Giving dexamethasone should reduce the levels of ACTH and cortisol due to negative feedback. But in people with cushings these levels remain high.

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40
Q

How to treat cushings?

A

Adrenalectomy if adrenal adenoma

Transsphenoidal surgical resection if pituitary adenoma

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41
Q

What are the complications of cushings?

A

Cardiovascular disease, hypertension, DM and osteoporosis

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42
Q

What is primary adrenal insufficiency?

A

Addisons disease, decreased production of cortisol

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43
Q

What is secondary adrenal insufficiency?

A

Decreased ACTH secretion, there is pituitary/hypothalamic involvement

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44
Q

What are the most common causes of addisons?

A

Autoimmune, can be caused by TB (developing countries)

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45
Q

Risk factors for addisons?

A

Female, adrenocortical antibodies, other autoimmune disease

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46
Q

Symptoms of addisons?

A

Fatigue, weakness, weight loss

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47
Q

Signs of addisons?

A

Hyper pigmentation, postural hypotension, hypoglycaemia

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48
Q

What are the sodium and potassium levels like in addisons?

A

Low sodium high potassium

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49
Q

Investigations for addisons?

A

FBC (anaemia and eosinophilia)

Morning serum cortisol reduced, adrenal CT or MRI

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50
Q

How to manage addisons?

A

Treat underlying cause, glucocorticoid+mineralocorticoid replaceent

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51
Q

What is Conn’s syndrome?

A

Autonomous aldosterone production that exceeds the body’s requirements

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52
Q

What is the pathophysiology of COnn’s?

A

Excess aldosterone
Increased Na reabsorptio and K+ excretion in the kidneys
Hypertension and potential hypokalemia

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53
Q

How do people with Conn’s present?

A

hypertension, nocturia and polyuria, mood disturbance, difficulty concentrating excessive thirst

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54
Q

Investigations for Conns

A

Low potassium, high aldosterone to renin ratio

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55
Q

How to treat Conns?

A

SPIRONOLACTONE aldosterone antagonist, lower BP, resolve electrolyte imbalance.

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56
Q

What is the definition of hypokalaemia?

A

Potassium levels lower than 3.5mmol/l

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57
Q

Symptoms of hypokalaemia?

A

Asymptomatic, fatigue, generalised weakness, muscle cramps and pain, palpitations

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58
Q

Signs of hypokalaemia

A

Arrhtthmias, muscle paralysis and rhabdomyolysis

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59
Q

What are the causes of hypokalaemia?

A

Increased excretion, reduced intake, shift to intracellular

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60
Q

Reasons for increased excretion o potassium?

A

Drugs (thiazide, loop dieuretics), Renal disease, GI loss, increased aldosterone

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61
Q

Which drugs cause a shift to intracellular K?

A

Insulin and salbutamol

62
Q

What ECG changes will you see in hypokalemia?

A

Flat T-waves, ST depression, prominent U waves, prolonged PR

63
Q

What other investigations to diagnose hypokalaemia?

A

Urine osmolality, electrolytes

bloods FBC and U&E

64
Q

What is the definitieon of hyeprkalaemia?

A

greater than 5.5mmol/L

65
Q

What are the symptoms of hyperkalaemia?

A

Fatigue, generalised weakness, chest pain, palpitations

66
Q

What are the signs of hyperkalemia?

A

Arrhythmias, reduced power, reduced reflexs,

67
Q

Causes of hyperkalemia?

A

AKI and CKD, drugs, renal tubular acidosis, metabolic acidosis

68
Q

What are the characteristics of hyperkalemia on ECG?

A

Tall tented T-waves

69
Q

How to manage hyperkalemia?

A

ABC assessment, consider cardiac monitoring,
protect myocardium with calcium gluconate
Drive K+ intracellulary with insulin/dextrose, salbutamol

70
Q

What is carcinoid syndrome?

A

Groups of symptoms due to release of serotonin and other vasoactive peptides into the systemic circulation from a carcinoid tumour .

71
Q

What are the symptoms of carcinoid syndroem?

A

diarrhoea and flushing

72
Q

What are the signs of carcinoid syndrome?

A

Palpitations, abdominal cramps, RHF, bronchospasm

73
Q

How would you investigate carcinoid?

A

High volumes of hydroxyindoleactic acid in the blood.

Metabolic panel and liver ultrasound to confirm mets

74
Q

How would you treat carcinoid?

A

Surgical ressection, radiofrequency ablation

75
Q

What is hyperthyroidism?

A

More thyroid hormone being made or released

76
Q

What is graves disease?

A

Antibodies binding to the TSH receptor causing more T3/T4 to be made

77
Q

What is toxic multinodular goitre?

A

Hyperthyroidism seen often in the elderly. Thyroid enlarges with lots of little nodules which release harmful amounts of TSH

78
Q

What are the causes of secondary hyperthyroidism?

A

Pituitary tumour

79
Q

What are the risk factors for hyperthyroidism?

A

Young/middle aged women, smokers, stress, HLA-DR3

80
Q

What are the symptoms of hyperthyroidism?

A

Hot and sweaty, diarrhoea, weight loss, anxiety/restlessness, hyperphagia.

81
Q

What are the signs of hyperthyroidism?

A

Periorbital swelling, goitre, tachycardia

82
Q

What are the investigations for hyperthyroidism?

A

Thyroid function tests

83
Q

What are the results of thyroid tests for primary hyperthyroidism?

A

High T3/4, low TSH in primary

84
Q

How to manage hyperthyroidism?

A

Propranolol for control of symptoms
Carbimazole
Surgery to remove nodules
Radioiodine

85
Q

What are the 2 regimes of carbimazole you can try?

A

Block and replace.

Titration according to TFT’s

86
Q

What is thyroid eye disease?

A

Eye discomfort, grittiness, photophobia, increased tear production

87
Q

What is Hashimotos thyroiditis?

A

Antibodies attack the thyroid causing inflammation and dysfunction, lowering T3/4 levels

88
Q

What are the risk factors for hypothyroidism?

A

Other autoimmune diseases, post partum

89
Q

Symptoms of hypothyroidism?

A

Weight gain, depression, constipaion, cold intolerance, brain fog

90
Q

What are the signs of hypothyroidism?

A

Bradycardia, delayed reflexes

91
Q

Investigations for hypothyroidism?

A

TFT’s

92
Q

TFT results for primary hypothyroidism?

A

Low T3/4 high TSH

93
Q

How to treat hypothyroidism?

A

Levothyroxine (T4)

94
Q

Complications of hypothyroidism?

A

Heart disease, pregnancy problems, coma

95
Q

Is there a goitre in primary atrophic hypothyroidism?

A

No goitre as there is atrophy of the thyroid gland

96
Q

Is there a goitre in Hashimotos thyroiditis?

A

Goitre due to lymphocytic and plasma cell infiltration

97
Q

What is the main cause of hypothyroidism worldwide?

A

Iodine deficiency

98
Q

What is acromegaly?

A

Too much growth hormone usually from a pituitary tumour

99
Q

What does growth hormone stimulate?

A

bone and muscle growth, increased protein synthesis, fat/glycogen breakdown

100
Q

What is GH converted into in the liver?

A

Insulin like growth factor 1

101
Q

Symptoms of acromegaly?

A

Large hands, box jaw, thick skin, arthritis, sight problems

102
Q

Signs of acromegaly?

A

Hypertension, insulin resistance, bitemporal hemiopia

103
Q

What does acromegaly cause bitemporal hemiopia?

A

A pituitary tumour compressing the optic chiasm

104
Q

What investigations would you do for acromegaly?

A

ILGF-1 blood test, ask about changes in shoe/ring size

105
Q

How would you manage acromegaly?

A

Tumour surgery, cabergoline (dopamine agonist), somatostatin analogue, GH receptor antagonist

106
Q

What are the complications of acromegaly?

A

Diabetes, sleep apnoea, heart disease

107
Q

What is a prolactinoma?

A

A tumour secreting prolactin

108
Q

What are the symptoms of a prolactinoma?

A

Amenorrhea, galactorrhoea, gynaecomastia, low libido, possible cerebral symptoms

109
Q

Signs of prolactinoma?

A

Infertility, low testosterone

110
Q

Investigations for prolactinoma?

A

Prolactin levels, CT head

111
Q

Management of a prolactinoma?

A

Surgery, carbergoline

112
Q

Complications of a prolactinoma?

A

Infertility, sight loss, raised intracranial pressure

113
Q

What is SIADH?

A

A condition where your body produces too much ADH

114
Q

What is the result of Too much ADH?

A

Water is absorbed back into the blood from the collecting duct

115
Q

What are the causes of SIADH?

A

Brain injury, infection, hypothyroidism, cancers, lung diseases

116
Q

Symptoms of SIADH?

A

N+V, headache, lethargy, cramps, weakness, confusion

117
Q

Signs of SIADH?

A

Raised JVP, oedema, ascites

118
Q

investigations for SIADH?

A

ADH levels, U&E’s low sodium normal potassium

119
Q

How to manage SIADH?

A

Fluid restriction, treat underlying cause, increase osmolarity

120
Q

What is diabetes insipidus?

A

Reduced ADH secretion causing large passage of dilute urine

121
Q

Symptoms of DI?

A

Polyuria, polydipsia

122
Q

Signs of DI?

A

Dry mucosa, sunken eyes, changes to skin turgidity

123
Q

What is cranial DI?

A

Hypothalamus doesnt produce enough ADH

124
Q

What is nephrogenic DI?

A

Kidneys do not respond to DI

125
Q

What investigations should you do for DI?

A

Water deprivation test, ADH suppression test

Urine dip for glucose

126
Q

How does the water deprivation test differentiate between cranial and nephrogenic?

A

When you give desmopressin in cranial the kidneys will respond to it and the osmolaritly will increase whereas with nephrogenic the osmolality won’t increase.

127
Q

How to manage DI?

A

Rehydration, desmopressin, thiazide diuretics

128
Q

What are the causes of hypocalcaemia?

A

Vit D deficiency, hypoparathyroidism, hypoventilation

129
Q

What is calcium used for in the body?

A

Neurotransmission and muscle contraction

130
Q

Symptoms of hypocalcaemia?

A

convulsions, arrhythmias, tetany and numbness

131
Q

Signs of hypocalcaemia?

A

Chevostek’s sign (tapping facial nerve induces spasm), BP cuff causes wrist to flex and fingers to draw together (trousseau’s

132
Q

Investigations for hypocalcaemia?

A

Corrected calcium levels, ECG (prolonged QT)

Parathyroid function

133
Q

How to treat hypocalcaemia?

A

10ml calcium gluconate/chloride, orla calcium and Vit D

134
Q

complications of hypocalcaemia?

A

Seizure, cardiac arrest

135
Q

Causes of hypercalcaemia ?

A

hyperparathyroidism, malignancy, sarcoidosis, thyrotoxicosis, drugs

136
Q

Symptoms of hypercalcaemia?

A

soft weak bones, abdo pain, N+V, constipation, depression

137
Q

Signs of hypercalcaemia?

A

Short QT and kidney stones

138
Q

Investigations for hypercalcaemia>

A

Corrected calcium levels, ECG and look for cause

139
Q

Management of hypercalcaemia>

A

treat underlying cause, increase circulation volume, increase excretion, bisphosphotes

140
Q

what is the function of PTH?

A

Increased calcium through bone resorption, gut absorption, renal absorption, and activates Vit D

141
Q

Risk factors for hyperparathyroidism?

A

Women 50-60 years

142
Q

Symptoms of hyperparathyroidism?

A

Bones, stones, groans and psychic moans

143
Q

Signs of hyperparathyroidism?

A

Hypercalcaemia

144
Q

Investigations for hyperpaathyroidism?

A

PTH bone profile, high TH low calcium phosphates, DEXA scan (salt and pepper degradation of bone

145
Q

Management of hyperparathyroidism?

A

Watchful waiting, surgery to remove the dodgy gland

146
Q

Cuases of hypoparathyroidism?

A

Autoimmune, congenital, acquired damage

147
Q

What does a bone profile show for hypoparathyroidism?

A

Low calcium, normal/high phosphate, low PTH

148
Q

State 3 types of cancers that cause SIADH?

A

Prostate cancer, small cell carcinoma, pancreatic cancer

149
Q

What is secondary adrenal insufficiency?

A

Caused by long term steroid therapy leading to suppression of the pituitary adrenal axis.

150
Q

Symptoms of secondary adrenal insufficiency?

A

tired, tearful, weakness, anorexia, dizziness

Phase 2a medicine (14 decks)

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