Endocrinology Flashcards
1
Q
Parathyroid hormone function
A
Raises calcium levels
2
Q
Secondary hyperparathyroidism
A
Low calcium triggers > High PTH > still Low calcium (due to secondary cause)
High phosphate
3
Q
Tertiary hyperparathyroidism
A
High PTH
High calcium
High phosphate
(Tertiary = 3)
4
Q
Primary hyperparathyroidism
A
High PTH
High calcium
Low phosphate
5
Q
Symptoms:
Low mood and energy
Constipation + abdominal pain
Dysuria
A
Hyperparathyroidism
hypercalcaemia = stones (urinary symptoms), bones (bone pain), moans (depression), groans (constipation)
6
Q
URGENT complication of CKD
A
HYPERKALAEMIA: arrhythmias (VT and VF)
Tx:
calcium gluconate (IF heart arrhythmias)
insulin + dextrose (1st line if no heart arrhythmias)
7
Q
43 year old man symptoms over last 3 months Polyuria Polydipsia Nocturia Unexplained weight loss
A
Diabetes Type II
8
Q
Diagnostic tests in DM2
A
NEED TWO ABNORMAL TESTS:
HbA1c >48
Fasting >7
Random >11
9
Q
Monitoring test in DM
A
HbA1c
10
Q
First line Mx in DM2
A
LIFESTYLE
11
Q
Sulfonylurea most dangerous side effect
A
hypoglycaemia
12
Q
Diabetes complications
A
Microvascular = OPATHY (retinopathy, peripheral neuropathy, nephropathy)
13
Q
First line in DKA after ABCs
A
IV fluids
14
Q
Diabetic ketoacidosis > Tx with high dose Insulin = fatigue, muscle cramping
Diagnosis? ECG pattern?
A
Insulin moves potassium into cells > HYPOKALAEMIA > U waves
15
Q
Most significant ECG pattern in HYPERKALAEMIA
A
Tall Tented T waves
16
Q
Diarrhoea not related to food intake + no blood/mucus
Facial flushing precipitated by stress
Intermittent palpitations
O/E: Hepatomegaly
A
Carcinoid tumour
GOLD STANDARD Ix: urinary 5-hydroxyindolecetic acid
Symptoms only appear when the tumour has metastasised to the liver (gets broken down elsewhere)
17
Q
Fatigue
Weight gain
Bitemporal hemianopia
PMH: DM T2
Diagnosis? Ix?
A
Acromegaly
1st line: IGF-1
GOLD STANDARD: OGTT
Growth hormone inhibits insulin from working (so you eventually develop insulin resistance) and increases gluconeogenesis
18
Q
Anxiety
Tremors
Palpitations
Weight loss
ECG: absent P waves, AF
Ix?
A
Hyperthyroidism: thyroid function test
19
Q
Young onset hypertension
Non responsive to medication
A
Conns syndrome
20
Q
Phaeochromocytoma Ix
A
Plasma free metanephrines
21
Q
Neck pain radiating to the jaw Palpitations Sweating Recently recovered from viral infection Raised ESR Normal TFT No weight loss
A
De Quervains thyroiditis
22
Q
Graves triad
A
opthalmopathy, dermopathy (pretibial myoexedema), acropachy (clubbing)
23
Q
Causes of drug induced Hyperthyroidism
A
Amiodarone + lithium
24
Q
Hyperthyroidism Tx principles
A
TITRATE + BLOCK (slowly increase dose of carbimazole)
BLOCK AND REPLACE (carbimazole > levothyroxine)
25
Signs of agranulocytosis from carbimazole
Sore throat
fevers
Ulcers
26
Most common cause of Cushing’s
EXOGENOUS STEROIDS
27
Endogenous causes of Cushing’s
Corticotropin dependent:
Pituitary adenoma
SCLC
Corticotropin independent:
Adrenal adenoma
28
Complications of Cushing’s
CVD
Hypertension
Type 2 Diabetes
Osteoporosis +/- fractures
Courtney Has Ten Owls🙄🦉
29
Addisons patho
Autoimmune damage of the adrenal glands
| Not enough cortisol = RAISED ACTH = pigmentation
30
Risk factors Addisons
```
FHx autoimmune
Female
TB
HIV (opportunistic infection)
Sarcoidosis
Adrenal haemorrhage
```
31
Diagnostic test Addisons
SynACTHen
Other Ix: 9am cortisol
32
Addisons U&Es
Low sodium
High potassium
- due to FALL IN ALDOSTERONE
33
Addisons treatment
Hydrocortisone
| Fludrocortisone (corrects glucocorticoids)
34
Carpal tunnel in acromegaly
Due to excess growth of hands
35
Complications of acromegaly
Diabetes T2
Cardiomyopathy
HTN
36
Severe abdo pain and weakness
Tachycardia, Low BP, Low urine output (hypovolaemic shock)
Hypoglycaemia
Deep pigmentation in buccal mucosa and skin creases
ADDISONIAN CRISIS
| Tx: IV hydrocortisone + saline to correct dehydration and hypotension
37
SIADH
| Diagnostic criteria:
Euvolemic hyponatraemia, High urine osmolality, Low plasma osmolality
38
Causes of SIADH
```
SCLC
Infection (pneumonia)
Abscess
Drugs e.g. SSRIs, sulfonylureas, carbamazepine
Head injury
Alcohol withdrawal
```
39
Diabetes insipidus
Neurogenic: Lack of production to ADH
Nephrogenic: Lack of response to ADH
Px: Polyuria, polydipsia without weight loss
Diagnostic test: water deprivation test (desmopressin stimulation test)
- neurogenic: decreased urine output
- nephrogenic: continued high urine output
40
Chvosteks sign
Clinical finding in HYPOCALCAEMIA
41
ADH MOA
Insertion of aquaporin channels
42
ADH effect on Na+ levels
Hyponatraemia: dilutes the level of Na+ in the blood
43
Causes of SIADH
44
Gold standard Ix in acromegaly
Oral glucose tolerance test (OGTT)
```
Measure glucose + GH
75g glucose
Measure GH response to glucose
- normal: GH decreases in response to glucose
- acromegaly: GH remains high
```
45
1st line screening test for acromegaly
Serum IGF-1
46
Hypercalcaemia ECG changes
Shortening of the QT interval (due to reduction in the calcium plateau of the action potential)
47
Hypercalcaemia Tx
Fluids
| Calcitonin + IV Bisphosphonates
48
Calcitonin
Hormone secreted by parafollicular cells in the thyroid to REDUCE CALCIUM LEVELS
49
Child on second level of asthma treatment ladder
| Weight gain but not height gain
ICS
| Iatrogenic Cushing’s syndrome
50
T1DM risk factors
HLA DR3/DQ2
HLA DR4/DQ8
Northern European
Other autoimmune diseases (90%)
51
T1DM epidemiology
Usually presents ages 5-15
| 10% of diabetes = T1
52
Processes STIMULATED by insulin
GLUT4 uptake into cells
Glycogenesis into glycogen (for storage in hepatocytes)
Additional glucose > converted to fatty acids (exported from hepatocytes as lipoproteins > storage in adipocytes)
53
Processes SUPPRESSED by insulin
Glycogenolysis (glucose from glycogen stores)
Gluconeogenesis (glucose from non-carb)
Lipolysis (release of free fatty acids from adipocytes) > Ketogenesis (acetyl coA to acidic ketone bodies)
= PATHOGENESIS OF DKA (LACK OF INSULIN IN T1DM)
54
T1DM diagnostic test
Random plasma glucose >11mmol/L
55
```
Polydipsia
Polyuria
Ketosis
Rapid weight-loss
Young
BMI <25
Personal or family history of autoimmune disease
```
T1DM
56
Pathological causes of T2DM
Increased insulin resistance +/- Reduced insulin secretion
Gestational diabetes
Steroids/Cushing’s
Chronic pancreatitis
57
T2DM risk factors
Lifestyle: obesity, sedentary, high calorie or alcohol excess
Higher prevalence in Asian men
Above 40 years old (late onset)
Hypertension
58
Why is weight loss characteristic of T1DM and not T2DM
Weight loss = muscle breakdown from loss of insulin (occurs later in most cases of T2DM, insulin resistance occurs first)
59
Second line Mx T2DM
Metformin (increases insulin sensitivity)
60
Metformin dual therapy options
DPP4 (depeptidyl peptidase) inhibitor
Sulfonylurea (gliclazide) - increases insulin SECRETION
Pioglitiazone
61
Why does hyperglycaemia cause dehydration
Osmotic diuresis
62
Signs of DKA
Kussmauls breathing
Pear drop breath
Hypotension
Tachycardia
63
DKA Ix
```
Random plasma glucose >11
Plasma ketones >3
Blood pH <7.35 or Bicarbonate <15
Urine dipstick: glucosuria, ketonuria
Serum U&E: raised urea + creatinine, decreased total K+, increased serum K+
```
64
DKA Tx
1. ABC management
2. IV fluids
3. IV insulin
4. restore electrolytes (e.g. K+)
65
Hyperosmolar hyperglycaemic state
Serious complication of T2DM
Hyperglycaemia = osmotic diuresis/high plasma osmolality
Enough insulin to prevent ketogenesis/DKA
Px: severe dehydration, confusion and reduced mental state
66
HSS Tx
IV fluids
Insulin (at low rate of infusion)
Restore electrolytes
LMWH
67
Hyperthyroidism epidemiology
Mainly young women 20-40 yrs (F > M 9:1)
| Graves’ disease = 65-75% of cases
68
Hyperthyroidism risk factors
Smoking
Stress
HLA-DR3
Other autoimmune diseases: T1DM, Addison’s, Vitiligo
69
Effects of increased T3
```
Increased:
metabolic rate
cardiac output
bone resorption
activation of sympathetic nervous system
```
70
Px of hyperthyroidism
EVERYTHING GOES FAST
71
Second line treatment in hyperthyroidism
Propylthiouracil (prevents T4 > T3 conversion)
72
Mechanism of action of carbimazole
Blocks synthesis of T4
73
Hyperthyroidism Tx options
1. Drug management: carbimazole, propylthiouracil; beta blockers for symptoms
2. Radioiodine
3. Thyroidectomy
74
Pathophysiology of Graves’ disease
IgG autoantibodies (anti-TSHR-Ab) bind to TSH receptors and increase T4/T3 production
Interaction with orbital autoantigens = thyroid eye disease
75
Graves specific symptoms
Thyroid eye disease (25-50%):
- eyelid retraction
- preorbital swelling
- proptosis/exopthlamos
Pretibial myxoedema
Thyroid acropachy
76
Hypothyroidism epidemiology
Mainly >40 years old
| F > M 6:1
77
Aetiology of hypothyroidism
```
Primary:
Autoimmune: Hashimotos, Atrophy
Iodine deficiency
Drugs
Post thyroidectomy
```
Secondary:
Hypopituitarism
78
Autoantibodies in Hashimotos
Anti-TPO
79
Signs of hypothyroidism
```
BRADYCARDIC
Bradycardia
Reflexes
Ataxia
Dry hair/skin
Yawning
Cold hands
Ascites
Round face (puffy)
Defeated demeanour
Immobile
Congestive cardiac failure
```
80
Cushing’s aetiology
ACTH dependent
- Cushing’s disease (pituitary adenoma)
- Ectopic ACTH (SCLC)
ACTH independent
- Iatrogenic
- Adrenal adenoma
81
Cushing’s Px
+ mood change, acne
82
Cushing’s Ix
Multiple investigations:
- Random plasma cortisol
- Overnight dexamethasone suppression test
- Urinary free cortisol (24 hour)
- Plasma ACTH
83
Dexamethasone suppression test
84
Causes of acromegaly
```
Pituitary adenoma (MOST COMMON = 99%)
Secondary to malignancy that secrets ectopic GH (SCLC)
```
85
Complications of acromegaly
Erectile dysfunction
| Diabetes Mellitus
86
Treatment of acromegaly
1st line: transsphenoidal resection surgery
2nd line: somatostatin analogue eg ocreotide
3rd line: GH receptor antagonist
4th line: dopamine agonist
87
Prolactinoma
Benign adenoma of pituitary gland producing excess prolactin
88
Galactorrhoea
Prolactinoma stimulates milk production from mammary gland as well as inhibiting FSH and LH
89
Prolactinoma Ix
Prolactin levels
| CT head
90
Gold standard Prolactinoma Tx
Transsphenoidal resection surgery of pituitary
91
1st line Prolactinoma Tx
Dopamine agonists (bromocriptine/carbergoline) - dopamine has an inhibitory effect on prolactin
92
Conns syndrome
Primary hyperaldosteronism due to an aldosterone producing adenoma = high sodium and water retention and increase potassium excretion independent of RAAS
93
Conns syndrome Px
```
HTN
Hypokalaemia
Nocturia
Polyuria
Mood disturbance
Difficulty concentrating
```
94
Conns syndrome Ix
Aldosterone:Renin ratio: increased
| U&Es (plasma potassium: decreased)
95
Conns syndrome Tx 1st line + gold standard
```
1st line (pre-operative)
Spironolactone (aldosterone antagonist) - controls HTN and K+
```
Gold standard: laparoscopic adrenalectomy
96
Addison’s disease
Primary adrenal insufficiency = destruction of adrenal cortex leads to decreased production of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
(opposite of Cushing’s and Conn’s)
97
Causes of Addison’s disease
Autoimmune destruction (80% of UK cases)
TB (most common cause worldwide)
Adrenal metastases
98
Presentation of Addison’s disease
```
Tanned
Lean
Fatigue
Pigmented palmar creases
Postural hypotension
```
99
Addison’s disease Ix 1st line + gold standard
1st line: U&E (hyponatraemia, hyperkalaemia, hypoglycaemia)
Gold standard: Short synACTHen test (high ACTH, low cortisol)
Plasma renin and aldosterone (high renin, low aldosterone)
Other tests:
Adrenal CT/MRI
21-hydroxylase adrenal autoantibodies (80% +)
100
Addison’s disease Tx
Steroid replacement dependent on Px:
- Hydrocortisone (cortisol replacement)
- Fludrocortisone (aldosterone replacement)
Treat underlying cause
STEROID WITHDRAWAL ADVICE
101
SIADH causes + Tx
Post-operative from major surgery
Infection (atypical pneumonia + lung abscess)
Head injury
Medications (thiazide diuretics) - MOST COMMON CAUSE
Tx = treat underlying cause e.g. stop medication
102
SIADH Px
```
Headache
Nausea
Fatigue
Muscle cramps
Confusion
Severe hyponatraemia
```
103
Tolvaptan
ADH receptor blocker, can be used in SIADH
104
Potassium normal range (mmol/L)
3.5-5.5
105
Causes of hyperkalaemia
1. IMPAIRED EXCRETION
- AKI/CKD
- Iatrogenic (ACEi, NSAIDs, Beta-blockers)
- Addison’s disease
2. INCREASED INTAKE
- IV K+ therapy
- dietary
3. SHIFT TO EXTRACELLULAR
- tumour lysis syndrome
- decreased insulin
- metabolic acidosis (H+/K+)
106
Px of potassium imbalance
```
Fatigue
Weakness
Cramping
Palpitations
Arrythmias
Hypotonia
Hyporeflexia
Paralysis
```
Hypo: constipation, Hyper: diarrhoea
107
Hyperkalaemia Tx
ABC
Cardiac monitoring
- if cardiac problems = calcium gluconate 1st line to protect myocardium
No cardiac problems = insulin + dextrose 1st line (or nebulised salbutamol) = drive K+ intracellularly
Treat underlying cause
108
Causes of hypokalaemia
1. INCREASED EXCRETION
- Renal disease
- Iatrogenic (thiazide, loop diuretics)
- GI loss (D+V)
- Conns syndrome (aldosterone)
2. DECREASED INTAKE
- dietary
3. SHIFT TO INTRACELLULAR
- metabolic alkalosis
- Iatrogenic (insulin, B2 agonists - SABA/LABA)
109
Hypokalaemia ECG changes
Prolonged PR interval
ST depression
Flat T waves
Prominent U waves
110
Causes of cranial diabetes insipidus
[DISRUPTED ADH SECRETION]
```
Idiopathic
Congenital
Tumour
Trauma
Infection
```
111
Causes of nephrogenic diabetes insipidus
[DISRUPTED ADH RESPONSE]
Inherited/genetic mutation
Metabolic
Iatrogenic (lithium)
Chronic renal disease
112
Gold standard diagnostic test for DI
8 hour water deprivation test
- measure plasma and urine osmolality
- end of 8h: desmopressin + measure plasma osmality (nephrogenic won’t react to ADH analogue)
113
Tx of Diabetes insipidus
Treat underlying cause
Conservative management - rehydration
Cranial: desmopressin to replace ADH
Nephrogenic: bendroflumethiazide
114
Ix to establish cranial vs nephrogenic DI
Desmopressin test
Nephrogenic: urine osmolality, urine output
Cranial: urine osmalility, urine output
115
Primary hyperPTH
Patho
Aetiology
Ix
Tx
1 PTH gland produces excess PTH
Adenomas (80%) or hyperplasia of all glands
Raised calcium
Surgical removal of adenoma, bisphosphonates
116
Secondary hyperPTH
Patho
Aetiology
Ix
Tx
Increased secretion of PTH to compensate hypocalcaemia
CKD/Low Vit D
Low serum calcium
Calcium correction, treat underlying cause
117
Tertiary hyperPTH
Patho
Aetiology
Ix
Tx
Autonomous secretion of PTH even after correction of calcium deficiency (due to CKD)
Prolonged secondary hyperparathyroidism
Raised calcium
Cinacalcet (calcium mimetic - reduces PTH levels), total/part parathyroidectomy
118
Hyperparathyroidism Px
```
Bones (bone pain)
Stones (renal calculi)
Moans (psychiatric)
Groans (abdominal)
Hypercalcaemia
```
119
Primary hypoPTH
= gland failure
Autoimmune destruction
Congenital (DiGeorge syndrome)
120
Secondary hypoPTH causes
```
Surgical removal
Decreased magnesium (required for PTH secretion)
```
121
HypoPTH symptoms
= neurones become more excitable
```
CATS go numb
Convulsions
Arrythmias
Tetany
Spasm
Numbness
```
122
HypoPTH signs
```
Chvosteks sign (facial nerve tap induces spasm)
Trousseaus sign (BP cuff causes wrist flexion and fingers to pull together)
```
123
Primary hypoPTH Ix
Decreased calcium, increased or normal phosphate, decreased PTH
ECG: prolonged QT + ST segments
124
Causes of hypercalcaemia
```
CHIMPANZEES
Calcium supplements
Hydrochlorothiazide
Iatrogenic/Immobilisation
Multiple Myeloma/Medication (lithiuM)
Parathyroid hyperplasia (primary)
Alcohol
Neoplasm
Zollinger Ellison syndrome
Excessive Vit D
Excess Vit A
Sarcoidosis
```
125
Triad of carcinoid symptoms
Palpitations
Diarrhoea
Flushing
126
Carcinoid syndrome patho
Enterochromoffin cell tumour producing 5-HT
Most commonly found in terminal ileum or appendix
Hepatic involvement = carcinoid SYNDROME
Excess secretion of substance P, insulin, 5-HTm ACTH, bradykinin etc - wide range of symptoms
127
Most common cause of secondary adrenal insufficiency
Long term corticosteroid use
128
Carcinoid immediate treatment
Somatostatin analogue + surgery
