Endocrine Flashcards

Question 1

Q

What is DM due to?

Answer

A

A lack of or reduced effectiveness of endogenous insulin

Question 2

Q

What does hyperglycaemia cause? (2)

Answer

A

) Microvascular problems

- ) Macrovascular problems

Question 3

Q

Give 2 microvascular problems

Answer

A

) Retinopathy
) Nephropathy
) Neuropathy

Question 4

Q

Give 2 macrovascular problems

Answer

A

) Stroke
) Renovascular disease
) Limb ischaemia
) Heart disease

Question 5

Q

When does T1DM usually present?

Answer

A

Adolescence

Question 6

Q

What causes T1DM?

Answer

A

Insulin deficiency from autoimmune destruction of insulin-secreting pancreatic beta cells

Question 7

Q

What is T1DM associated with?

Answer

A

Other autoimmune diseases

Question 8

Q

What autoimmune genes are present in 90% of T1DM cases?

Answer

A

HLA DR3 +/- DR4

Question 9

Q

Which gene determines islet sensitivity to damage?

Question 10

Q

What is latent autoimmune diabetes of adults (LADA) a form of?

Question 11

Q

What is metabolic syndrome?

Answer

A

Central obesity (BMI >30) with 2 of:

) BP >130/85
) Triglycerides >1.7mmol/L
) HDL <1.2mmol/L
) Fasting glucose >5.6mmol/L
) DM

Question 12

Q

In who is T2DM more prevalent? (3)

Answer

A

) Asians
) Men
) Elderly

Question 13

Q

What causes T2DM?

Answer

A

Decreased insulin secretion +/- increased insulin resistance

Question 14

Q

Give 2 things T2DM is associated with

Answer

A

) Obesity
) Lack of exercise
) Calorie excess
) Alcohol excess

Question 15

Q

Which type of DM has a stronger genetic influence?

Question 16

Q

What does T2DM typically progress from? (2)

Answer

A

) Impaired glucose tolerance

- ) Impaired fasting glucose

Question 17

Q

What is maturity onset diabetes of the young (MODY)?

Answer

A

A rare autosomal dominant form of T2DM affecting young people

Question 18

Q

Give 3 other causes of DM

Answer

A

) Steroids
) Anti HIV drugs
) Newer antipsychotics
) Pancreas (pancreatitis, surgery, trauma, CF, haemochromatosis, cancer)
) Cushing’s disease
) Acromegaly
) Phaeochromocytoma
) Hyperthyroidism
) Pregnancy
) Congenital lipodystrophy
) Glycogen storage diseases

Question 19

Q

How do we diagnose DM?

Answer

A

-) Symptoms of hyperglycaemia
-) Raised venous glucose detected once
OR
-) Raised venous glucose on 2 separate occasions OR
-) Oral glucose tolerance test (OGTT)
WITH
-) HbA1c

Question 20

Q

Give 3 symptoms of hyperglycaemia

Answer

A

) Polyuria
) Polydipsia
) Unexplained weight loss
) Visual blurring
) Genital thrush
) Lethargy

Question 21

Q

What values do we need for a raised venous glucose?

Answer

A

) Fasting >7mmol/L

- ) Random >11.1mmol/L

Question 22

Q

What values do we need for an OGTT?

Answer

A

2 hour valve of >11.1mmol/L

Question 23

Q

What value do we need for HbA1c?

Answer

A

> 48mmol/mol

Question 24

Q

What does HbA1c measure?

Answer

A

Average 3 month plasma glucose concentration, glycated Hb

Question 25

Q

Give 3 features of T1DM

Answer

A

) Weight loss
) Persistent hyperglycaemia despite diet and medications
) Autoantibodies (islet cell, anti-glutamic acid decarboxylase)
) Ketonuria

Question 26

Q

How do we monitor glucose control? (3)

Answer

A

) Fingerprick glucose (before informs about long acting, after - short acting)
) HbA1c
) Hypoglycaemic attacks

Question 27

Q

What is the general control of DM?

Answer

A

) Lifestyle changes
) Address vascular risk factors
) Diabetic reviews
) Foot and eye care
) Inform DVLA

Question 28

Q

Give 2 lifestyle changes for DM treatment

Answer

A

) Smoking cessation
) Low carbohydrate or ketogenic diet
) Low glycemic index foods
) Weight loss
) Exercise

Question 29

Q

How do we treat T1DM?

Answer

A

) Insulin (short, medium, long acting)
) Self adjust doses with excessive, fingerprick glucose, calorie intake, carb counting
) Avoid binge drinking
) Give surgary drinks if hypoglycaemic attack

Question 30

Q

Give 3 common insulin regimens

Answer

A

) BD biphasic, twice daily premixed insulins by pen
) QDS, before meals ultra fast and bedtime long acting
) Once daily before bed long acting

Question 31

Q

What are the treatment steps for T2DM?

Answer

A

1) Lifestyle modification
2) Metformin
3) Dual therapy, add DPP4 inhibitor or pioglitazone or sulphonylurea or SGLT-2i
4) Triple therapy
5) Insulin or metformin, sulphonylurea and GLP 1 mimetic

Question 32

Q

What is metformin?

Answer

A

A biguanide that increases insulin sensitivity and helps weight

Question 33

Q

How do DPP4 inhibitors/gliptins work?

Answer

A

Block the action of DPP-4, an enzyme which destroys the incretin hormone

Question 34

Q

How does glitazone work?

Answer

A

Increases insulin sensitivity

Question 35

Q

How does sulfonylurea work?

Answer

A

Increases insulin secretion

Question 36

Q

How does SGLTI work?

Answer

A

Selective sodium-glucose co-transporter-2 inhibitor, blocks reabsorption of glucose in kidneys and promotes excretion of excess glucose in urine

Question 37

Q

Give 3 complications of DM

Answer

A

) MI
) Stroke
) Cataracts
) Nephropathy
) Retinopathy (blindness)
) Foot ulcers

Question 38

Q

What can we use to stop the progression of diabetic retinopathy?

Answer

A

Laser photocoagulation

Question 39

Q

What does laser photocoagulation do? (DM)

Answer

A

Stops production of angiogenic factors from the ischaemic retina

Question 40

Q

What are the 4 types of diabetic retinopathy?

Answer

A

) Background
) Pre-proliferative
) Proliferative
) Maculopathy

Question 41

Q

How do we distinguish between ischaemia and peripheral neuropathy in diabetics feet?

Answer

A

Ischaemia - critical toes +/- absent foot pulses

Peripheral neuropathy - injury/infection over pressure points

Question 42

Q

How do we treat neuropathy complications?

Answer

A

) Relieve pressure
) Antibiotics for infections
) Dressings

Question 43

Q

What is ketoacidosis?

Answer

A

An alternative metabolic pathway used in starvation states, less efficient

Question 44

Q

What does ketoacidosis produce as a by-product?

Question 45

Q

How does ketoacidosis occur in diabetics? (4)

Answer

A

) Excessive glucose
) Cannot be taken up into cells due to lack of insulin
) Body into starvation like state
) Ketoacidosis only mechanism of energy production

Question 46

Q

Give 4 clinical features of diabetic ketoacidosis

Answer

A

) Gradual drowsiness
) Vomiting
) Dehydration
) Abdo pain, polyuria, polydipsia, lethargy, anorexia, ketotic breath, dehydration, coma, deep breathing

Question 47

Q

What type of DM does diabetic ketoacidosis usually affect?

Question 48

Q

Give 3 triggers of diabetic ketoacidosis

Answer

A

) Infection
) Surgery
) MI
) Pancreatitis
) Chemotherapy
) Antipsychotics
) Wrong insulin dose
) Non compliance

Question 49

Q

What 3 things do we diagnose diabetic ketoacidosis with?

Answer

A

) Acidaemia
) Hypergylcaemia
) Ketonaemia

Question 50

Q

What tests do we do in diabetic ketoacidosis?

Answer

A

) ECG
) CXR
) Dipstick
) MSU
) Glucose
) Ketones
) pH
) U&E
) HCO3-
) Osmolality
) FBC
) Blood cultures

Question 51

Q

Give 3 things that would make diabetic ketoacidosis severe

Answer

A

) Very high ketones
) Low venous bicarbonate
) Low pH
) Low K
) Low GCS
) Low O2
) Low systolic BP
) Pulse high/low
) High anion gap

Question 52

Q

What is the management of diabetic ketoacidosis? (8)

Answer

A

) Saline bolus
) Tests
) IV insulin and aim for fall in blood ketones or rise in venous bicarbonate
) Potassium if needed
) Consider catheter, NG
) LMWH
) Avoid hypoglycaemia by giving glucose when <14mmol/L
) Treat cause

Question 53

Q

What type of DM does hyperglycaemic hyperosmolar state usually affect?

Question 54

Q

What is hyperglycaemic hyperosmolar state?

Answer

A

Longer history with marked dehydration and glucose, no switch to ketone metabolism

Question 55

Q

What do we give in hyperglycaemic hyperosmolar state?

Answer

A

LMWH as occlusive events are a danger

Question 56

Q

How do we treat hyperglycaemic hyperosmolar state?

Answer

A

) Fluid
) K+ when urine flows
) Maybe insulin
) Treat cause

Question 57

Q

What does hypoglycaemia present with?

Answer

A

) Odd behaviour
) Sweating
) Increased pulse
) Seizures

Question 58

Q

How do we treat hypoglycaemia?

Answer

A

) Conscious - quick acting carb snack
) Conscious but uncooperative - glucose gel in mouth
) Unconscious - glucose IVI or glucagon

Question 59

Q

What is a phaeochromocytoma?

Answer

A

Rate catecholamine producing tumours

Question 60

Q

What do phaeochromocytoma arise from?

Answer

A

Sympathetic paraganglia cells (phaeochrome bodies), which are collections of chromatin cells

Question 61

Q

Where are phaeochromocytomas usually found?

Answer

A

Within the adrenal medulla

Question 62

Q

Where are rarer extra-adrenal phaeochromocytomas found?

Answer

A

By the aortic bifurcation

Question 63

Q

What is the 10% rule of phaeochromocytomas? (4)

Answer

A

10% malignant
10% extra-adrenal
10% bilateral
10% familial

Question 64

Q

Give a gene that is mutated in phaeochromocytoma

Answer

A

SDH, succinyl dehydrogenase

Answer 59

A

Hereditary cancer syndromes:

) Thyroid
) MEN-2A and 2B
) Neurofibromatosis
) von Hippel-Lindaue syndrome

Answer 60

A

) Episodic headache
) Sweating
) Tachycardia

Answer 61

A

) Difficult to control BP
) Palpitation
) High pulse
) Dyspnoea
) Angina
) Headache
) Anxiety

Answer 62

A

) Metanephrines/metadrenaline in 25h urine
) Increased WCC
) Abdominal CT/MRI to localise

Answer 63

A

) Surgery
) Alpha blockade pre-op
) With beta-blocker if heart disease or tachycardia
) Chemo if malignancy

Answer 64

A

GFR=MINER-GA
Zona glomerulosa - mineralocorticoids
Zona fasciculata - glucocorticoids
Zona reticularis - androgens

Answer 65

A

An increased secretion of growth hormone from a pituitary tumour or hyperplasia

Answer 66

A

Bone and soft tissue growth through increased secretion of insulin like growth factor 1

Answer 67

A

) Acroparaesthesia
) Amenorrhoea
) Loss of libido
) Headache
) Sweating
) Snoring
) Arthralgia
) Backache
) Skin darkening
) Goitre
) Malocclusion of jaw
) Increased size of hands and feet and face
) Curly hair
) Weight gain
) Oily large pored skin
) Scalp folds
) Gigantism if before bony epiphyses fuse

Answer 68

A

) High glucose, calcium, phosphate
) GH secretion fails to be suppressed by high glucose (OGTT)
) MRI of pituitary fossa
) Hypopituitarism
) Visual fields and acuity
) ECG
) Old photos

Answer 69

A

) Transphenoidal surgery to prevent compression
) Somatostatin analogues or radiotherapy if surgery doesn’t work
) Growth hormone antagonist pegvisomant if resistant/intolerant to somatostatin analogue

Answer 70

A

Hyperthyroidism

Answer 71

A

) Circulating IgG autoantibodies bind to and activate G protein coupled thyrotropin receptors
) Smooth thyroid enlargement
) Increases hormone production (especially T3)
) React with orbital autoantigens

Answer 72

A

) Vitiligo
) T1DM
) Addison’s

Answer 73

A

) Stress
) Infection
) Childbrith

Answer 74

A

) Diarrhoea
) Weight loss
) Increased appetite
) Sweats
) Heat intolerance
) Tremor
) Oligomenorrhoea
) Subfertility
) Eye disease
) Oedema above ankles
) Clubbing

Answer 75

A

) TSH suppressed
) T4 and T3 high
) Maybe mild normocytic anaemia or mild neutropenia
) High ESR
) High caclium
) High LFT

Answer 76

A

) Beta blockers
) Carbimazole to titrate against TH levels
) Can block replace - carbimazole and thyroxine
) Radioiodine or thyroidectomy if relapse

Answer 77

A

) Lethargy
) Low mood
) Dislike of cold
) Increased weight
) Constipation
) Menorrhagia
) Dementia
) Myalgia
) Cramps
) Bradycardic symptoms

Answer 78

A

) Slow relaxation of reflexes
) Ataxia
) Dry thin hair/skin
) Cold hands
) Ascites
) Round puffy face
) Defeated demeanour
) Immobile
) Congestive HF

Answer 79

A

) TSH high
) T4 low
) Autoantibodies if Hashimoto’s

Answer 80

A

Hashimoto’s thyroiditis

Answer 81

A

Swelling of the neck due to lymphocytic and plasma cell infiltration

Answer 82

A

Women, 60-70

Answer 83

A

Hypothyroid or euthyroid

Answer 84

A

Young and healthy - levothyroxine (T4)

Elderly/comorbid - lower dose of levothyroixine

Answer 85

A

Angina or MI

Answer 86

A

) T3, T4, TSH, thyroid autoantibodies
) CXR may show tracheal goitres and mets
) US, fine needle aspiration, cytology
) Radionuclide scans may show malignant lesions as hypofunctioning/cold (hyperfunctioning/hot suggests adenoma)

Answer 87

A

) Papillary (60%)
) Follicular (<25%)
) Medullary (5%)
) Lymphoma (5%)
) Anaplastic (rare)

Answer 88

A

Younger patients, to lymph nodes and lungs

Answer 89

A

) Total thyroidectomy
) +/- node excision
) +/- radioiodiine
) Levothyroxine

Answer 90

A

Middle aged, via blood to bone and lungs

Answer 91

A

) Total thyroidectomy
) T4 suppression
) Radioiodine ablation

Answer 92

A

Sporadic or part of MEN syndrome

Answer 93

A

Calcitonin (can be used as tumour marker)

Answer 94

A

) Phaeochromocytoma scan pre-op
) Thyroidectomy
) Node clearance
) Maybe beam radiotherapy to prevent recurrance

Answer 95

A

Females, stridor or dysphagia

Answer 96

A

Histology for MALT

Answer 97

A

Mucosa-associated lymphoid tissue

Answer 98

A

Chemoradiotherapy

Answer 99

A

Rare, females more, elderly

Answer 100

A

Clinical state produced by:

) Chronic glucocorticoid excess
) Loss of normal feedback mechanisms of hypothalamo-pituitary-adrenal axis
) Loss of circadian rhythm of cortisol secretion

Answer 101

A

Oral steroids

Answer 102

A

Increased adrenocorticotropic releasing hormone (ACTH) due to pituitary adenoma (Cushing’s disease)

Answer 103

A

Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma

Answer 104

A

) Weight gain
) Mood change
) Proximal weakness
) Gonadal dysfunction
) Acne
) Recurrent Achilles tendon rupture

Answer 105

A

) Central obesity
) Plethoric moon face
) Buffalo hump
) Supraclavicular fat distribution
) Skin and muscle atrophy
) Bruises
) Purple abdominal striate
) Osteoporosis
) Increased BP
) Increased glucose
) Infection prone
) Poor healing

Answer 106

A

) Raised plasma cortisol
) Overnight dexamethasone suppression test (no suppression by cortisol)
) 24hr free cortisol
) 48hr dexamethasone suppression test

Answer 107

A

) Plasma ACTH (undetectable, adrenal tumour likely)
) CT/MRI adrenal glands
) Adrenal vein sampling
) High dose suppression test if ACTH detectable
) Cortisol rises with pituitary disease but not with ectopic ACTH production
) MRI pituitary

Answer 108

A

) Iatriogenic - stop medications
) Cushing’s disease - selective removal of pituitary adenoma, bilateral adrenalectomy if unlocatable or recurrence
) Adrenal tumour - adrenalectomy, radiotherapy if carcinoma
) Ectopic ACTH - surgery

Answer 109

A

A solitary aldosterone producing adenoma that causes primary hyperaldosteronism

Answer 110

A

Excess production of aldosterone independent of the renin-angiotensin system

Answer 111

A

Increased sodium and water retention, and decreased renin release

Answer 112

A

) Asymptomatic
) Signs of hypokalaemia
) Weakness
) Cramps
) Paraesthesiae
) Polyuria
) Polydipsia
) Increased BP sometimes

Answer 113

A

) U&E
) Renin
) Aldosterone
) Adrenal vein sampling

Answer 114

A

) Laparoscopic adrenalectomy

- ) Spironolactone for 4wks pre-op to control BP and K+

Answer 115

A

Addison’s disease

Answer 116

A

Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency

Answer 117

A

) Autoimmunity
) TB
) Adrenal mets
) Lymphoma
) Opportunistic infections in HIV
) Adrenal haemorrhage
) Congenital

Answer 118

A

Iatrogenic - due to long term steroid therapy leading to suppression of the pituitary-adrenal axis

Answer 119

A

On withdrawal of steroids

Answer 120

A

) Toned/lean
) Tanned
) Tired
) Tearful
) Possible weakness, anorexia, dizzy, faints, flu-like myalgia/arthralgias
) Depression, psychosis
) N&V, abdominal pain, diarrhoea/constipation
) Pigmented palmar creases
) Buccal mucosa
) Postural hypotension
) Vitilago

Answer 121

A

) Decreased sodium
) Increased potassium
) Low glucose
) Ureaemia
) High calcium
) Eosinophilia
) Anaemia

Answer 122

A

Addison’s

Answer 123

A

Short ACTH stimulation test

) Plasma cortisol before and 30mins after tetracosactide
) Exclude Addison’s if cortisol high
) Also test renin and aldosterone if high

Answer 124

A

) 21-hydroxylase adrenal autoantibodies

- ) CT, CXR for TB, mets

Answer 125

A

) Replace steroids with daily hydrocortisone
) Mineralocorticoids correct postural hypotension, low Na+, high K+ (fludrocortisone)
) Steroid use bracelet
) Double steroids in febrile injury, stress, illness

Answer 126

A

The passage of large volumes of dilute urine due to impaired water resorption by the kidney

Answer 127

A

Cranial DI - reduced ADH secretion from the posterior pituitary
Nephrogenic DI - impaired response of kidney to ADH

Answer 128

A

) Idiopathic
) Congenital
) Tumour
) Trauma
) Hypophysectomy
) Autoimmune hypophysitis
) Infiltration
) Vascular
) Infection

Answer 129

A

) Inherited
) Metabolic (low K, high Ca)
) Lithium
) Chronic renal disease
) Post obstructive uropathy

Answer 130

A

) Polyuria
) Polydipsia
) Dehydration
) Symptoms of hypernatraemia

Answer 131

A

) U&E
) Ca
) Glucose
) Serum and urine osmolalities
) Water deprivation test

Answer 132

A

Dilute, despite raised plasma osmolality (U:P>2)

Answer 133

A

Urine osmolality increases after desmopressin in cranial DI

Answer 134

A

) MRI
) Test anterior pituitary function
) Desmopressin

Answer 135

A

) Treat cause
) Bendroflumethiazide if persists
) NSAIDs low urine volume and plasma Na+

Answer 136

A

Hyponatraemia

Answer 137

A

) Concentrated urine
) Hyponatraemia
) Low plasma osmolality
) In absence of hypovolaemia, oedema, diuretics

Answer 138

A

) Malignancy (SCLC, pancreas)
) CNS disorders (meningoencephalitis, absess, stoke)
) Chest disease (TB, pneumonia)
) Endocrine disease (hypothyroidism)
) Drugs (opiates, SSRIs)
) Other (trauma, surgery, HIV)

Answer 139

A

) Treat cause
) Restrict fluid
) Consider salt +/- loop diuretic if severe
) Possible vasopressin receptor antagonists

Answer 140

A

> 6.5mmol/L

Answer 141

A

) Fast irregular pulse
) Chest pain
) Weakness
) Palpitations
) Light headedness

Answer 142

A

) Tall tented T waves
) Small P waves
) Wide QRS complex
) Ventricular fibrillation

Answer 143

A

) Haemolysis
) Contamination with potassium EDTA anticoagulant
) Delayed analysis

Answer 144

A

) Oliguric renal failure
) K+ sparing diuretics
) Rhabdomyolysis
) Metabolic acidosis
) Excess K+ therapy
) Addison’s
) Massive blood transfusion
) Burns
) Drugs
) Artefactual result

Answer 145

A

) Treat cause
) Review medications
) Polystyrene sultanate resin (binds to K+ in gut)

Answer 146

A

Digoxin toxicity

Answer 147

A

) Muscle weakness
) Hypotonia
) Hyporeflexia
) Cramps
) Tetany
) Palpitations
) Light-headedness
) Constipation

Answer 148

A

) Small or inverted T waves
) Prominent U waves
) Long PR interval
) Depressed ST segments

Answer 149

A

) Diuretics
) Vomiting and diarrhoea
) Pyloric stenosis
) Rectal villous adenoma
) Intestinal fistula
) Cushing’s syndrome/steroids/ACTH
) Conn’s syndrome
) Alkalosis
) Purgative and liquorice abuse
) Renal tubular failure

Answer 150

A

Increased bicarbonate

Answer 151

A

Low Mg2+ levels

Answer 152

A

) Oral K+ supplement

- ) Consider K+ sparing diuretic

Answer 153

A

Give IV potassium slowly

Answer 154

A

Bones, stones, groans, psychic moans

) Abdominal pain
) Vomiting
) Constipation
) Polyuria
) Polydipsia
) Depression
) Anorexia
) Weight loss
) Tiredness
) Weakness
) HTN
) Confusion
) Pyrexia
) Renal stones
) Renal failure
) MI

Answer 155

A

Decreased QT interval

Answer 156

A

) Malignancy
) Primary hyperparathyroidism
) Sacoidosis
) Vitamin D intoxication
) Thyrotoxicosis
) Lithium
) Tertiary hyperparathyroidism
) HIV

Answer 157

A

) Decreased albumin
) Decreased chloride
) Alkalosis
) Decreased potassium
) Increased phosphate
) Increased ALP

Answer 158

A

Increased PTH

Answer 159

A

) FBC
) Protein electrophoresis
) CXR
) Isotope bone scan
) 24hr urinary Ca2+ excretion

Answer 160

A

) Treat cause
) Correct dehydration
) Bisphosphonates (prevent bone resorption)
) Chemo for malignancy
) Steroids for sarcoidosis

Answer 161

A

SPASMODIC

) Spasms
) Perioral paraesthesia
) Anxious, irritable, irrational
) Seizures
) Muscle tone increased in smooth muscle (wheeze, dysphagia, colic)
) Orientation impaired and confusion
) Dermatitis
) Impetigo herpetiformis
) Chvostek’s sign, choreoathetosis, cataract, cardiomyopathy

Answer 162

A

Long QT interval

Answer 163

A

Tapping over the parotid/facial nerve makes the facial muscles twtich

Answer 164

A

) CKD
) Hypoparathroidism (& pseudo)
) Acute rhabdomyolysis
) Hypomagnesaemia

Answer 165

A

) Vitamin D deficiency
) Osteomalacia
) Acute pancreatitis
) Over-hydration
) Respiratory alkalosis

Answer 166

A

) Mild - daily calcium
) CKD - alfacalcidol
) Severe - calcium glutamate IV

Answer 167

A

Gland failure

Answer 168

A

) Decreased Ca
) Increased/normal phosphate
) Normal ALP

Answer 169

A

) Those of hypocalcaemia (SPASMODIC)

- ) Autoimmune signs

Answer 170

A

) Autoimmune

- ) Congenital

Answer 171

A

Calcium supplements and calcitriol

Answer 172

A

) Radiation
) Surgery
) Hypomagnesaemia

Answer 173

A

Failure of the target ell to respond to PTH

Answer 174

A

Low ionised calcium levels

Answer 175

A

Negative feedback via calcium levels

Answer 176

A

) Increases osteoclast activity releasing calcium and phosphate from bones
) Increases calcium and decreases phosphate reabsorption in the kidney
) Increases active 1,25-dihydroxyvitamin D3 production

Answer 177

A

Increased calcium and decreased phosphate

Answer 178

A

) Solitary adenoma (80%)
) Hyperplasia of all glands
) Parathyroid cancer

Answer 179

A

MEN, multiple endocrine neoplasia

Answer 180

A

) Increased calcium - weak, tired, depressed, thirsty, polyuric, renal stones, abdominal pain, pancreatitis, ulcers
) Bone reabsorption - pain, fractures, osteopenia/porosis
) Increased BP

Answer 181

A

Calcium levels

Answer 182

A

) Increased calcium
) Increased PTH
) Decreased phosphate
) Increased ALP (from bone activity)
) 24hr urinary calcium increased
) Imaging shows bone lesions
) DEXA

Answer 183

A

) Mild - increase fluid, avoid thiazides and high calcium/vitamin D intake
) Excision of adenoma/all 4 hyperplastic glands
) Cinacalcet

Answer 184

A

Increases sensitivity of parathyroid cells to calcium

Answer 185

A

) Hypoparathyroidism
) Recurrant laryngeal nerve damage
) Symptomatic calcium decrease

Answer 186

A

Calcium is decreased and PTH is increased

Answer 187

A

Decreased vitamin D intake, chronic renal failure

Answer 188

A

) Treat causes
) Phosphate binder
) Vitamin D
) Cinacalcet if PTH very high

Answer 189

A

Calcium is increased and PTH is very high

Answer 190

A

Prolonged secondary hyperparathyroidism, causing the glands to act autonomously having undergone hyper plastic or adenomatous change

Answer 191

A

Increased secretion of PTH unlimited by feedback control

Answer 192

A

Chronic renal failure

Answer 193

A

Occurs in 5% of carcinoid tumours, implying hepatic involvement

Answer 194

A

A diverse group of tumours of enterochromaffin cell (neural crest) origin capable of producing 5HT (serotonin)

Answer 195

A

) Appendix (45%)
) Ileum (30%)
) Rectum (20%)
) GI tract, ovary, testis, bronchi

Answer 196

A

) Initially few
) GI tumours - appendicitis, intussusception, obstruction
) Hepatic tumours - RUQ pain

Answer 197

A

) Bradykinin
) Tachykinin
) Substance P (pain)
) VIP
) Gastrin
) Insulin
) Glucagon
) ACTH (Cushing’s syndrome)
) PTH
) THs

Answer 198

A

) Bronchoconstriction
) Paroxysmal flushing in upper body
) Diarrhoea
) CCF

Answer 199

A

Tricuspid incompetence and pulmonary stenosis from 5HT induced fibrosis

Answer 200

A

) Increased 24hr 5HIAA
) CXR and chest/pelvis MRI/CT to localise
) Plasma chromogranin A (tumour mass)

Answer 201

A

5-hydroxyindoleacetic acid, 5HT metabolite

Answer 202

A

) Octerotide
) Treat symptoms
) Resection to cure

Answer 203

A

Somatostatin analogue that blocks

Answer 204

A

A disorder of the pilosebaceious follicles

Answer 205

A

Occurs as a result of androgenic simulation on the sebaceous gland causing excessive sebum, outflow obstruction, leakage into dermis and infection with propionibacterium acnes (skin commensal), leads to inflammation

Answer 206

A

Greasy skin and lesions
-) Open comedones (blackheads)
-) Closed comedones (whiteheads)
-) Papules (deep)
-) Pustules (more superficial)
-) Nodules
-) Cysts
On face, chest, neck, back

Answer 207

A

) Wash twice daily with soap/acne soap and water
) Topical treatments
) Systemic treatments

Answer 208

A

Encourage skin peeling, reduce inflammation, have antibiotic effect

Answer 209

A

) Benzoyl peroxide
) Clindamycin/erythromycin
) Retinoids

Answer 210

A

) Antiobiotics oxytetracycline, clindamycin, erythromycin
) Isotrenoin
) Antiandrogens (e.g. pill)

Answer 211

A

SEs include severe drying of skin and possible depressive effects

Answer 212

A

IgE mediated T cell autoimmune response to allergens

Answer 213

A

Increased cleanliness so decreased germ exposure in early life results in over production of pro allergy T cells

Answer 214

A

) Rash (inside of elbows, knees, around eyes and neck)

- ) Pruritus

Answer 215

A

) Dry air
) Sweating
) Local irritation
) Stress

Answer 216

A

First 3 months of life

Answer 217

A

Chronic relapsing/remitting course (but usually improves throughout childhood)

Answer 218

A

) Lichenification

- ) Infection

Answer 219

A

The skin becomes thick and leathery as a result of epidermal hypertrophy from excessive scratching

Answer 220

A

Staphylococcus

Answer 221

A

) Remove precipitating factors
) Emollients
) Steroid creams
) Antibiotics for infections
) Immune modulating agents
) Phototherapy
) Systemic steroids

Answer 222

A

An autoimmune disease characterised by patches of abnormal skin (genetic disease triggered by environmental factors)

Answer 223

A

Keratinocyte hyperproliferation

Answer 224

A

Basal layer to horny layer

Answer 225

A

) Classical
) Guttate
) Palmoplanar pustular
) Flexoral
) Erythrodermic

Answer 226

A

Well circumscribed erythematous plaques with silver scaling (itchy)

Answer 227

A

Elbow, knees, scalp

Answer 228

A

Children following strep throat

Answer 229

A

Yellow brown pustules on palms and soles

Answer 230

A

Erythematous but not scaly

Answer 231

A

Submammary, axially, anogenital

Answer 232

A

An acute onset of erythroderma, medical emergency

Answer 233

A

) Classical itchy painful patches
) Nails - pitting, lifting off bed, subungal hyperkeratosis
) Psoriatic arthritis possible

Answer 234

A

) Trauma
) Stress
) Sunlight
) Some drugs (NSAIDs, ACEIs)

Answer 235

A

) Emollients
) Topical corticosteroids
) Vitamin D analogues
) Coal tar preparations
) Dithranol cream
) Keratolytics
) Retinoids (topical/systemic)
) Immunosuppression
) Phototherapy if resistant

Answer 236

A

Decrease cell proliferation

Answer 237

A

Inhibit DNA synthesis

Answer 238

A

Decreases cell proliferation

Answer 239

A

Bacterial infection involving the inner layers of the skin

Answer 240

A

Group A strep or staph entering via a break in the kin

Answer 241

A

) Blistering
) Bite
) Pruritic rash
) Eczema
) Dry skin
) Injections
) DM
) Obesity

Answer 242

A

) Age

- ) Immunodeficiency

Answer 243

A

) Area of skin is red, hot, painful
) Lethargy possible
) Fever possible

Answer 244

A

Legs and face

Answer 245

A

) Antibiotics - flucloxacillin

- ) Surgical draining if abscess

Answer 246

A

Rapidly progressive infection of the deep fascia causing necrosis of subcutaneous tissue

Answer 247

A

) Group A beta haemolytic streptococci

- ) Often polymicrobial

Answer 248

A

Intense pain over skin surface of affected area and underlying muscle

Answer 249

A

) Radical debridement of dead tissue
) Amputation if gangrene
) IV antibiotics (benzylpenicillin and clindamycin)

Answer 250

A

Abnormal breaks in an epithelial surface

Answer 251

A

) Venous disease (70%)
) Arterial and venous disease (15%)
) Arterial disease (2%)
) Neuropathic
) Infective
) Traumatic
) Vasculitis

Answer 252

A

Ankle brachial pressure index ABPI

Answer 253

A

) Treat cause
) Prevention (smoking, nutrition, DM control)
) 4 layer compression bandaging if arterial pulse ok
) Debridement and gels for necrosis
) Antibiotics for infection

Answer 254

A

) Age
) Sun bed use
) Fair skin
) History of sunburn or living overseas
) FHx
) Phototherapy

Answer 255

A

Younger patients

Answer 256

A

Short period of intense UV exposure

Answer 257

A

Skin mole changes

Answer 258

A

Major - change in size, shape, colour

Minor - inflammation, sensory change, large, irregular colour, irregular border

Answer 259

A

Skin mole changes:

) Asymmetry
) Border irregular
) Colour non-uniform
) Diameter large
) Elevation

Answer 260

A

) Superficial spreading (70%)
) Nodular (10-15%)
) Lentigo (15%)

Answer 261

A

Grow slowly and met later

Answer 262

A

Invade deeply and met early

Answer 263

A

Usually on the face of elderly patients, large, flat and dark

Answer 264

A

) Early excision can be curative with wide margins

- ) Chemo for mets

Answer 265

A

Ulcerated lesion with hard, raised edges in sun exposed sites

Answer 266

A

Solar keratoses (crumbly, yellow white crusts)

Answer 267

A

) Lips of smokers

- ) In long standing ulcers

Answer 268

A

Local destruction may be extensive but metastasis is rare

Answer 269

A

Excision with radiotherapy for recurrence/nodes

Answer 270

A

Nodular or superficial

Answer 271

A

) Pearly nodule with rolled telangiectatic edge
) Face/sun exposed site
) May have central ulcer
) Mets rare

Answer 272

A

) Red scaly plaques with raised smooth edge
) Trunk or shoulders
) Usually due to UV exposure
) Excision, cyrotherapy
) Topical flurouracil or imiquimod cream

Answer 273

A

Causes necrosis and healing of cancerous skin and leaves normal skin unharmed

Answer 274

A

A group of disorders characterised by extracellular deposits of a protein in abnormal fibrillar form that is resistant to degradation

Answer 275

A

AL and AA

Answer 276

A

) AD
) T2DM
) Haemodialysis related amyloidosis

Answer 277

A

Biopsy of affected tissue with positive staining under a polarised light microscopy

Answer 278

A

1-2 years

Answer 279

A

The proliferation of a plasma cell clone leading to amyloidogenic monoclonal immunoglobulins and fibrillary light chain protein deposition

Answer 280

A

Organ failure and death

Answer 281

A

Myeloma and lymphoma

Answer 282

A

) Optimise nutrition
) Oral melphalan and prednisolone extends survival by months
) High dose IV melphalan and autologous peripheral blood stem cell transplant

Answer 283

A

Glomerular lesions - proteinuria and nephrotic syndrome

Answer 284

A

Restrictive cardiomyopathy, arrhythmias, angina

Answer 285

A

Peripheral and autonomic neuropathy, carpal tunnel syndrome

Answer 286

A

Macroglossia (big tongue), malabsorption, weight loss, perforation, haemorrhage, obstruction, hepatomegaly

Answer 287

A

Purpura, especially periorbital

Answer 288

A

Amyloid is derived from serum amyloid A, an acute phase protein, reflecting chronic inflammation in RA, UC, Crohn’s, chronic infections (TB, OM, bronchiectasis)

Answer 289

A

Kidneys, liver, spleen

Answer 290

A

) Proteinuria
) Nephrotic syndrome
) Hepatosplenomegaly

Answer 291

A

Manage underlying condition

Answer 292

A

Secondary

Answer 293

A

Autosomal dominant condition that usually causes a sensory or autonomic neuropathy

Answer 294

A

) Fibroadenoma
) Breast cysts
) Intraductal papilloma

Answer 295

A

Benign overgrowth of collagenous mesenchyme of one breast lobule

Answer 296

A

Usually <30 but can be up to menopause

Answer 297

A

Firm, smooth, mobile lump, painless, may be multiple

Answer 298

A

) Observe and reassure
) US and fine needle aspiration if doubt
) Surgical excision if large

Answer 299

A

A benign fluid filled rounded lump not fixed to surrounding tissue, occasionally painful

Answer 300

A

Common >35, especially perimenopausal

Answer 301

A

Aspiration

Answer 302

A

Aspirate if large

Answer 303

A

Benign breast lesion

Answer 304

A

) Near nipple (solitary, more near menopause)

- ) Peripheral breast (multiple, more in younger, associated with higher chance of malignancy)

Answer 305

A

Bloody nipple discharge

Answer 306

A

Galactogram

Answer 307

A

Microdochectomy excision

Answer 308

A

) Family history
) Age
) Long uninterruped oestrogen exposure
) Nulliparity/first pregnancy >30, not breastfed
) Early menarche and late menopause
) HRT, pill
) BRCA genes, act breast cancer
) Obesity

Answer 309

A

) Non-invasive ductal carcinoma in situ
) Non-invasive lobular carcinoma in situ
) Invasive ductal carcinoma
) Invasive lobular carcinoma
) Medullary cancers
) Colloid/mucoid
) Papillary
) Tubular
) Paget’s of the nipple

Answer 310

A

Invasive ductal carcinoma

Answer 311

A

Microcalcification

Answer 312

A

Medullary

Answer 313

A

Colloid/mucoid

Answer 314

A

Oestrogen receptor positive

Answer 315

A

Overexpression of HER2 (growth factor receptor gene)

Answer 316

A

) Clinical examination
) Radiology by US and mammography
) History and cytology by fine needle aspiration or core biopsy

Answer 317

A

1) Confined to breast, mobile
2) With lymph nodes in ipsilateral axilla
3) Tumour fixed to muscle but not chest wall, ipsilateral nodes make be fixed, skin involved
4) Complete fixation to chest wall, distant mets

Answer 318

A

) Wide local excision
) Mastectomy
) With axillary node sampling/clearance or sentinel node biopsy

Answer 319

A

) Radiotherapy

- ) Adjuvant chemotherapy

Answer 320

A

) Tamoxifen (blocks oestrogen)

- ) Aromatase inhibitors (blocks peripheral oestrogen synthesis)

Answer 321

A

) Ovarian ablation

- ) Gonadotropin releasing hormone analogues

Answer 322

A

Perception (trastuzumab) with chemo

Answer 323

A

CNS surgery or radiotherapy with bisphosphonates for bone protection

Answer 324

A

) Tissue expanders
) Implants
) Latissimus dorsi flap
) Transverse abdominis myocutaneous flap

Answer 325

A

Arm lymphoedema

Answer 326

A

Endocrine - secretions into the blood stream

Exocrine - glands through a duct to site of action

Answer 327

A

Thyroid, adrenal

Answer 328

A

Blood bourne, acting at distant sites

Answer 329

A

Acting on adjacent cells

Answer 330

A

Feedback on the same cell that secreted the hormone

Answer 331

A

In vesicles

Answer 332

A

Nope, synthesised on demand

Answer 333

A

Synthesis - preprohormone to pro hormone
Packaging - prohormone to hormone
Storage - hormone
Secretion - hormone

Answer 334

A

In pulses/bursts

Answer 335

A

Normetanephrines and metanephrines in the blood/urine - breakdown products

Answer 336

A

Adrenal medulla

Answer 337

A

Increases the conversion of norepinephrine to epinephrine

Answer 338

A

To the nucleus

Answer 339

A

Anterior - endocrine outpouching

Posterior - continuous projection from hypothalamus (hypothalamus synthesises, posterior pituitary releases)

Answer 340

A

) TSH - thyroid
) ACTH - adrenal cortex
) FSH and LH - testes/ovaries
) Growth hormone - entire body
) Prolactin - mammary glands

Answer 341

A

1) Hypothalamus secretes TRH
2) Anterior pituitary secretes hormones
3) Affects thyroid gland
4) Thyroid hormones produced
Negative feedback loops at each step

Answer 342

A

) Accelerates food metabolism
) Increased protein synthesis
) Stimulation of carbohydrate metabolism
) Enhances fat metabolism
) Increase in ventilation rate
) Increase in CO and HR
) Brain development during foetal life and postnatal development
)Growth rate accelerated

Answer 343

A

GFR
Zona glomerulosa
Zona fasciculata
Zona reticularis

Answer 344

A

Zona glomerulosa - mineralcorticoids, aldosterone
Zona fasciculata - glucocorticoids, cortisol
Zona reticularis - androgens, dehydroepiandosterone
Adrenal medulla - stress hormones, epinephrine

Answer 345

A

Adenohypophysis

Answer 346

A

Neurohypophysis

Answer 347

A

Portal venous circulation from the hypothalamus

Answer 348

A

) Pressure on local structures (optic nerves)
) Pressure on normal pituitary (hypopituitarism)
) Functioning tumour (Cushing’s, acromegaly)

Answer 349

A

Hypothyroidism

Answer 350

A

Thyroglobulin and thyroid peroxidase

Answer 351

A

Autoimmune, thyroid stimulating antibodies

Answer 352

A

) Stress
) High iodine intake
) Smoking

Answer 353

A

Swelling in extraocular muscles due to autoantigen in muscle crossreacting with thyroid autoantigen

Answer 354

A

An excess of thyroid hormones in the blood

Answer 355

A

) Overproduction
) Leakage of preformed hormone from thyroid
) Ingestion of excess thyroid hormone

Answer 356

A

) Grave’s disease
) Toxic multinodular goitre
) Toxic adenoma

Answer 357

A

Common presentation of adrenal insufficiency

Answer 358

A

) Hypotension
) Cardiovascular collapse
) Fatigue
) Fever
) Hypoglycaemia
) Hyponatraemia
) Hyperkalaemia

Brainscape's Knowledge GenomeTM

Endocrine Flashcards

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