Brainscape's Knowledge GenomeTM

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


See full index

3B > Endocrine 1 > Flashcards

Endocrine 1 Flashcards

1
Q

Adrenal cortex structure and function

A

Go Fetch Rex, Makes Good Sex

Zona Glomerulosa - Mineralocorticoids - ALDOSTERONE
Zona Fasciculata - Glucocorticoids - CORTISOL
Zona Reticularis - Sex hormones - Androgens - TESTOSTERONE

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

Renin

A

Secreted by juxtaglomerular cells
In response to low BP - SNS activation
Converts ANGIOTENSINOGEN to AT1

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

Angiotensin

A

AT1 converted to AT2 by ACE (from lungs)

Causes systemic vasoconstriction
Stimulates thirst centres in brain
Causes CV hypertrophy
Stimulates ZG to produce ALDOSTERONE

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

Aldosterone

A

Secreted by zona Glomerulosa
Acts on DCT and collecting ducts
Increases SODIUM reabsorption
Increases POTASSIUM excretion

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

ADH - Vasopressin

A

Secreted by PP - In response to low BP
Acts on collecting ducts
Increases water reabsorption

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

Hypervolaemic state

Hypertension

A

Cardiac distension
Raised AT2

Atrial myocytes secrete ANP

  • Vasodilation
  • Inhibits RENIN production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Addison’s aetiology

A

Primary adrenal insufficiency

Primary HYPOaldosteronism - AI

TB
Metastatic disease
HIV

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

Addison’s presentation

A

TTTT
Thin, Tanned, Tired, Tearful

N/V
Dizziness
Fatigue

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

Addison’s investigations

A

Bloods - U+E, FBC, serum CORTISOL

Short synACTHen test

  • Give ACTH
  • Should stimulate an increase in CORTISOL
  • Will not happen in Addison’s

CT adrenals

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

Addison’s clinical findings

A

Low CORTISOL

  • HYPOglycaemia
  • HYPERpigmentation - Palmar creases, joints, buccal mucosa

Low ANDROGENS

Low BP
Low SODIUM
High POTASSIUM

Metabolic acidosis

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

Addison’s management

A

Replace Mineralocorticoids - FLUDROCORTISONE
Replace Glucocorticoids - HYDROCORTISONE

Vaccinations

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

Addison’s - Adrenal crisis precipitants

A

Infection
Missed medication
Stress
Surgery

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

Addison’s - Adrenal crisis presentation

A

Abdo pain
Cramps
Fatigue

Very low BP - Circulatory collapse

Metabolic acidosis

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

Addison’s - Adrenal crisis management

A

IV FLUDROCORTISONE

IV HYDROCORTISONE

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

Cushing’s aetiology

A

Gushing CORTISOL

ACTH dependent

  • Pituitary tumour - Increased ACTH
  • Ectopic - SCLC

ACTH independent

  • Adrenal tumour
  • Exogenous CORTISOL - Steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cushing’s signs and symptoms

A

BBIIGGGG

Bone - Osteoporosis and fractures
Blood pressure ^^^

Infections
Irritability

GLUCOSE ^^^
Gynaecomastia
GnRH inhibition - Amenorrhoea
Gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cushing’s - Gluconeogenesis signs

A

Buffalo hump
Moon face

Diabetes
Central obesity
Muscle wasting
Abdominal striae

Thick skin
Bruising

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

Cushing’s investigations

A

24hr urinary free CORTISOL
ACTH levels - Low in ACTH independent

DEX suppression test - Low dose
- DEX will not suppress CORTISOL in Cushing’s

DEX - High dose

  • Differentiate between pituitary and ectopic
  • Suppression of Cortisol = Pituitary problem
  • NO suppression of cortisol = Ectopic problem

MRI adrenals
CT pituitary and thorax (SCLC)

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

Cushing’s management

A

Treat cause

  • Tumour excision
  • Steroid reduction

KETOCONAZOLE and METYRAPONE
- Decrease CORTISOL production

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

Conn’s aetiology

A

Primary HYPERaldosteronism

Primary - Low RENIN

  • Idiopathic
  • Adenoma

Secondary - High RENIN

  • Chronically low BP
  • Cardiac failure
  • Liver cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Conn’s presentation

A

High ALDOSTERONE
High BP
High SODIUM

Low POTASSIUM

  • Cramps
  • Weakness
  • Paraesthesia

Metabolic alkalosis

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

Conn’s investigations

A

ALDOSTERONE:RENIN ratio

Primary - High ALDOSTERONE and low RENIN

Secondary - High ALDOSTERONE and high RENIN

CT adrenals

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

Conn’s management

A

ALDOSTERONE antagonist - SPIRONOLACTONE

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

HYPERcalcaemia aetiology

A

METASTASES
MYELOMA

Granulomatous disease
TB/Sarcoidosis

HYPERthyroidism
HYPERparathyroidism

Dehydration
Addison’s

Drugs

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

HYPERcalcaemia presentation

A 
Bones - Bone pain 
Stones - Renal stones 
Groans - Abdominal pain 
Moans - Depression 
Thrones - Polydipsia, polyuria, constipation

Short QT

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

HYPERcalcaemia investigations and management

A

ECG - Short QT!

Calcium profile - Including vitamin D

HyperPTH screen

  • PTH ^ - Should be LOW if Calcium ^
  • Low phosphate
  • Tech-99 scan - PTH gland

Skeletal survey
CXR - TB/sarcoid

Myeloma screen - Protein electrophoresis / ESR

Management

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

HYPOcalcaemia aetiology

A

Diet - Vitamin D deficiency
Malabsorption

HYPOparathyroidism - Secondary HYPERparathyroidism

Renal disease
Acute pancreatitis

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

HYPOcalcaemia presentation

A 
Tetany - Chvostek sign 
Weakness 
Paraesthesia - Peri-oral
Trosseau's sign- Abnormal hand posturing with BP cuff
Long QT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

HYPOcalcaemia investigations

A 
Serum CALCIUM 
PTH 
U+E
CRP
Faecal calprotectin
Anti-TTG
30
Q

HYPOcalcaemia management

A

Calcium supplementation - ADCAL
IV CALCIUM GLUCONATE - Risk of tissue necrosis

Treat cause

31
Q

Acromegaly aetiology

A

Abnormal GH secretion

Pituitary adenoma

32
Q

Acromegaly presentation

A

Bitemporal hemianopia - Tunnel vision
Headaches
Dizziness

Greasy skin
Sweating

Large facial features
Large square hands
Large feet
Carpal tunnel

Diabetes
HTN

33
Q

Acromegaly investigations

A

IGF-1

MRI pituitary

34
Q

Acromegaly management

A

Somatostatin analogue - OCTREOTIDE

Transspenoidal tumour resection

35
Q

HYPERkalaemia aetiology

A

Addison’s
Rhabdomyolysis
AKI
Metabolic acidosis

Drugs

  • SPIRONOLACTONE
  • ACE-I
  • ARB
  • HEPARIN
36
Q

HYPERkalaemia presentation

A

Weakness
Fatigue
Flaccid paralysis
Decreased reflexes

37
Q

HYPERkalaemia investigations

A

ECG - TTT

Tall Tented T waves 
Absent P waves 
Broad QRS 
Long PR 
Sinusoidal wave 
VT
38
Q

HYPERkalaemia management

A

C BBIG, K DRop

CALCIUM GLUCONATE

  • Cardiac membrane protection
  • Only give if K > 6.5 or ECG signs
  • Can cause tissue necrosis
Beta agonist - SALBUTAMOL
Bicarbonates - SODIUM BICARBONATE
INSULIN - Moves POTASSIUM back into cells 
GLUCOSE - DEXTROSE
Diuretics - Eliminate POTASSIUM
Renal dialysis
39
Q

HYPOkalaemia aetiology

A

FUROSEMIDE
THIAZIDES

Conn’s
N/V
DKA management - INSULIN

40
Q

HYPOkaelaemia presentation

A

Weakness
Hypotonia
Cramps
Paraesthesia

41
Q

HYPOkalaemia investigations

A

ECG

Inverted T waves
Prolonged PR
U waves
ST depression

42
Q

HYPOkalaemia management

A

Oral POTASSIUM - SANDOK

43
Q

SIADH aetiology

A

Ectopic secretion - SCLC
Lung - TB, pneumonia
Brain - Meningitis, stroke, abscess
Drugs - Carbamazepine

44
Q

SIADH pathophysiology

A 
ADH made in hypothalamus 
Secreted by PP 
Binds to V2 receptors
Increases number of aquaporin-2 channels in collecting tubule
Leads to increased reabsorption of water
45
Q

SIADH presentation

A

Irritability
Muscle cramps
Tremor

46
Q

SIADH investigations

A

Low serum osmolality
High urine osmolality

Identify cause

  • CT head
  • CXR
47
Q

SIADH management

A

SLOW TO AVOID CENTRAL PONTINE MYELINOLYSIS

Treat cause
Restrict fluids
HYPERTONIC SALINE
DEMECLOCYCLINE

48
Q

Diabetes insipidus aetiology

A

Cranial

  • Pituitary tumour
  • Trauma
  • Surgery

Nephrogenic

  • CKD
  • LITHIUM
  • Low POTASSIUM
  • High CALCIUM
49
Q

Diabetes insipidus presentation

A

Low ADH
Polydipsia
Polyuria
Postural HYPOtension

50
Q

Diabetes insipidus investigations

A

High serum osmolality
Low urine osmolality

DESMOPRESSIN stimulation test

  • Cranial - Change in osmolality
  • Nephrogenic - Unable to respond - No change in osmolality

Find cause - Imagine

51
Q

Diabetes insipidus management

A

Cranial - DESMOPRESSIN

Nephrogenic - THIAZIDES + low salt diet

Treat cause

52
Q

Pheochromocytoma aetiology

A

MEN-2

Malignant proliferation of chromaffin cells
Production of catecholamines

53
Q

Pheochromocytoma presentation

A

TRIAD!

  1. Headaches
  2. Sweating
  3. Palpitations

HTN
Cafe au lait spots

54
Q

Pheochromocytoma investigations

A

24hr Metanephrines
24hr catecholamines

MRI adrenal medulla

55
Q

Pheochromocytoma management

A

ALPHA-BLOCKER
BETA-BLOCKER

Tumour resection

56
Q

Thyroid structure and function

A

Hypothalamus secretes TRH
AP secretes TSH
Thyroid produces T3 and T4

T3 and T4…

  • Regulate use of energy sources
  • Protein synthesis
  • Control body’s sensitivity to other hormones
57
Q

Classification of thyroid disorders

A

HYPOthyroidism

  • Primary - Problem affecting thyroid galnd
  • Secondary - Problem with pituitary
  • Congenital

HYPERthyroidism

  • Primary
  • Secondary < 1%
58
Q

HYPOthyroidism aetiology

A

Hashimoto’s thyroiditis

  • AI disease associated with DM1, Addison’s or pernicious anaemia
  • Transient thyrotoxicosis in acute phase

Drugs

  • LITHIUM
  • AMOIDARONE

Subacute thyroiditis - de Quervain’s
- Associated with painful goitre and raised ESR

Iodine deficiency - Most common cause in developing world

59
Q

HYPERthyroidism aetiology

A

Graves’ disease

  • Most common cause of thyrotoxicosis
  • May be associated with thyroid eye disease

Toxic multinodular goitre
- Autonomously functioning thyroid nodules that secrete excess thyroid hormones

Drugs - AMOIDARONE

60
Q

HYPOthyroidism presentation

A

Weight gain
Lethargy
Cold intolerance

Dry cold yellow skin
Non-pitting oedema - Hands and face
Dry coarse scalp hair
Loss of lateral aspect of eyebrows

Constipation
Menorrhagia

Decreased deep tendon reflexes
Carpal tunnel syndrome

61
Q

HYPERthyroidism s/s

A

Weight loss
Restlessness
Heat intolerance

Palpitations
Arrhythmias - AF?

Sweating
Pretibial myxoedema
Thydoid acropachy - Clubbing

Diarrhoea

Anxiety
Tremor

62
Q

TFTs

Graves’ disease
Primary HYPOthyroidism
Secondary HYPOthyroidism

A

Graves’

  • Low TSH
  • High T4

Primary HYPOthyroidism

  • High TSH
  • Low T4

Secondary HYPOthyroidism

  • Low TSH
  • Low T4
63
Q

Sick euthyroid syndrome

A

Low TSH
Low T4

Common in hospital inpatients
Changes reversible upon recovery from systemic illness

No treatment required

64
Q

Subclinical hypothyroidism

A

High TSH
Normal T4

Patients on their way to developing HYPOthyroidism

65
Q

Poor THYROXINE compliance

A

High TSH
Normal T4

Patients only taking THYROXINE in the days before a routine blood test

T4 normal but TSH lags - Reflects long-term low T4 levels

66
Q

Thyroid disorders- Additional investigations

A

Autoantibodies

  • Hashimoto’s - Anti-thyroid peroxidase (TPO)
  • Graves’ - TSH receptor antibodies
  • Thyroglobulin antibodies

Nuclear scintigraphy - Toxic multinodular goitre reveals patchy uptake

67
Q

Thyroid disorder management

A

HYPOthyroidism - LEVOTHYROXINE

HYPERthyroidism

  • Propranolol - Control symptoms
  • CARBIMAZOLE
  • Radioiodine treatment
68
Q

HYPOnatraemia definitions

A

Normal SODIUM = 135-145

HYPOnatraemia < 135
Severe < 125

Acute < 48 hours
Chronic > 48 hours

69
Q

HYPOnatraemia aetiology

A

EXCESS WATER

HYPOvolaemic
EUvolaemic
HYPERvolaemic

70
Q

HYPOnatraemia presentation

A

Chronic - Asymptomatic

Acute moderate

  • Headache
  • Irritability
  • N/V
  • Confusion/delirium
  • Unsteady gait

Acute severe

  • Stupor/coma
  • Convulsions
  • Respiratory arrest
71
Q

HYPOnatraemia - Effect on the brain

A

Low serum osmolality
Water moves into the brain causing swelling

Loss of SODIUM, POTASSIUM, CHLORINE, to compensate

72
Q

HYPOnatraemia management

A

HYPER or EUvolaemic = Fluid restriction

HYPOvolaemic = SALINE replacement

3B (23 decks)

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