Brainscape's Knowledge GenomeTM

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


See full index

MRCS Critical care > Critical care endocrine > Flashcards

Critical care endocrine Flashcards

1
Q

What do blood tests show in addisons?

A

Low sodium
High potassium
High ACTH
Low cortisol

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

How would you confirm diagnosis of addison’s?

A

Short synacthen test
Synacthen (ACTH analogue) normally causes increase in cortisol
Does not occur in addison’s

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

How would you manage hypotensive pt with suspected addison’s?

A

Resuscitate according to CCRISP protocol
15L O2
IV access, bloods (FBC, U+E, CRP, ACTH, Cortisol–> if possible before starting tx
IVI
IV hydrocortisone
Monitor blood glucose

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

What are the causes of addison’s disease?

A

Addison’s disease
-Congenital adrenal hyperplasia
-autoimmune adrenalitis

Addisonian crisis
-Iatrogenic (e.g. withdrawal high dose steroids)
-Surgery
-Trauma
-Infection

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

Describe layers of adrenal gland and function

A

Zona glomerulosa (mineralocorticoids–> aldosterone)
Zona reticularis (glucocorticoids –> cortisol)
Zona fasciculata (oestrogens and androgens –> oestriol, progesterone, testosterone)

Medulla (catecholamines–> adrenaline)

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

Where is ACTH released from?

A

Anterior pituitary

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

What is addison’s disease?

A

-Also known as primary adrenal insufficiency
-Characterised by inadequate production of aldosterone and cortisol by two outer layers adrenal cortex

Addison’s disease, also known as primary adrenal insufficiency,[4] is a rare long-term endocrine disorder characterized by inadequate production of the steroid hormones cortisol and aldosterone by the two outer layers of the cells of the adrenal glands (adrenal cortex), causing adrenal insufficiency
-Addison’s refers specifically to primary adrenal insufficiency rather than iatrogenic

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

What hormones are produced by pituitary?

A

Anterior: growth hormone, ACTH, TSH, FSH, LH, prolactin

Intermediate lobe: MSH (melanocyte stimulating hormone)

Posteiror: ADH, oxytocin

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

Describe actions of glucocorticoids:

A

Cardiovascular:
–> increases myocardial contractility
–> increases vasoconstriction

Immune system
–> antiinflammatory
–> immunosuppressive

Metabolism:
–Increases gluconeogenesis and glycogenolysis during fasting
-Increases glycogen storage during feeding

Bones
–Increases bone resorption and risk of fracture

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

Pituitary axis for cortisol and thyroid hormone

A

Hypothalamus –> Pituitary –> adrenal cortex
CRH –> ACTH –> cortisol
TRH–> TSH –> T3, T4

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

What would be your differential for pathological fracture with hypercalcaemia?

A

-Hypercalcaemia secondary to hyperparathyroidism
-metastases
-Multiple myeloma

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

Which cells release PTH?

A

Chief cells within parathyroid gland

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

What are the actions of PTH?

A

Kidney:
–> Increased calcium absorption in distal tubule
–> Decreased phosphate absorption in proximal and distal tubule
–> Increased 1 alpha hydroxylase, causing production 1,25 dihydroxyvitamin D: increased calcium resorption in small intestine

Bone:
–> increased action of osteoclasts: increased release of calcium and phosphate from bone

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

What is primary hyperparathyroidism?

A

-Excess parathyroid production by parathyroid gland
-May be due to adenoma or carcinoma
-PTH produced regardless of calcium level

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

What is secondary hyperparathyroidism?

A

-Excess PTH production in response to low calcium state e.g. renal failure
-PTH production in response to low ca

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

What is tertiary hyperparathyroidism

A

-Caused by hyperplasia parathyroid gland following secondary hyperparathyroid
-PTH produced in response to normal ca

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

What are functions of calcium

A

-Bone formation and maintenance
-Muscle contraction

-Any process involving exocytosis
-cofactor for certain clotting factors
-Regulation of intracellular proteins

18
Q

Why can you have temporary hypocalcaemia following parathyroidectomy for hyperparathyroid?

A

-‘hungry bone disease’
-Excess PTH causes leaching of calcium from bone
-When stimulus removed bone ‘mops up’ excess calcium, leading to temporary hypocalcaemia

19
Q

Describe symptoms high calcium

A

Stones, bones, moans, thrones, muscle tone
-Kidney stones
-Bone pain
-Abdominal pain
-Constipation and excessive urination
-Muscle weakness

Also
-Dehydration
-Vomiting
-Renal failure
-Dro

20
Q

Symptoms low calcium

A

“CATs go numb”
-convulsions
arrhythmias
-tetany
-numbness in the hands and feet and around the mouth

21
Q

What are the causes hypercalcaemia

A

Hypercalcaemia of malignancy
Multiple myeloma
Hyperparathyroid

Familial Hypocalcuric hypercalcaemia
Paget’s disease
Sarcoidosis

22
Q

What would you get on hypercalcaemia vs hypocalcaemia ecg?

A

Hyper: u have no pot and no t but a long pr and short qt

Shortened qt

Hypo

U have no pot and no t but a long pr and qut

U wave
T wave inversion
Long PR
Long QT

23
Q

Describe DKA

A

-Breakdown of fatty acids due to lack of insulin
-Causes production of ketone bodies
-Produces triad of hyperglycaemia, acidosis and ketosis

24
Q

Describe management of DKA

A

-Manage according to ccrisp protocols
-fixed rate insulin infusion (0.1 unit/kg/hr)
-Give IVI
-Hourly monitoring of blood glucose and ketones
-Regular monitoring electrolytes and ph
-Monitor conscious level (deterioration may be sign of co2 rise or cerebral oedema)
-VTE prophylaxis
-Contact diabetes team

25
Q

What are causes DKA?

A

Sepsis
Surgery
MI
stress (e.g. trauma)
Non compliance with insulin therapy

26
Q

How would you manage pt with T1 diabetes in pre, perioperative and post operative setting?

A

Pre op: First on list, VRII from midnight if missing >1 meal, regular monitoring BMs
Intra op: Continue VRII, regular monitoring BMs,
Post op: regular monitoring BMs, continue VRII until eating and drinking normally

27
Q

What are the functions of pancreas?

A

Exocrine: proteolytic, lipolytic enzymes and amylase
Endocrine: secrete insulin, glucagon, somatostatin

28
Q

Where are endocrine hormones produced in pancreas?

A

4 types of islets of langerhans
-Beta cells: insulin
-Alpha cells: glucagon
-Delta cells: somatostatin
-gamma cells: pancreatic polypeptide

29
Q

What is addison’s disease?

A

-primary adrenal insufficiency
-Characterised by inadquate production of cortisol and aldosterone by two outer layers adrenal cortex

Addison’s disease, also known as primary adrenal insufficiency,[4] is a rare long-term endocrine disorder characterized by inadequate production of the steroid hormones cortisol and aldosterone by the two outer layers of the cells of the adrenal glands (adrenal cortex), causing adrenal insufficiency

30
Q

What are the features of myxoedema coma?

A

-Altered mental state/coma
-Hypothermia
-Bradycardia
-Hypoglycaemia

31
Q

What are the causes of myxoedema coma?

A

Undiagnosed hypothyroidism
Failure to comply with regular levothyroxine

32
Q

How do patient’s with hypothyroidism present?

A

Symptoms
-Weight gain
-Cold intolerance
-Decreased appetite
-Constipation
-Depression
-Fatigue

Signs
-Bradycardia
-Dry skin
-Loss of outer 1/3rd of eyebrow

33
Q

What would you find on examination in hypothyroidism?

A

Bradycardia
Slowed reflexes
Goitre
Dry skin
Loss outer 1/3rd eyebrow

34
Q

Describe anatomy of thyroid gland

A

Structure
-2 lobes with isthmus overlying 2nd-4th tracheal rings
-Each lobe is 5-6cm in length, 2.5-3cm in width. C5-T1 vertebral levels
-Surrounded by pretracheal fascia

Blood supply
-Superior thyroid artery, branch of external carotid
-Inferior thyroid, branch of thyrocervical trunk
-Occasionally thyroid IMA from brachiocephalic trunk or aortic arch

Venous drainage:
-Superior and middle thyroid veins –> drain to internal jugular vein
-Inferior thyroid vein –> drains to brachiocephalic vein

35
Q

Name hormones produced by thyroid gland:

A

-Thyroxine
-Tri-iodothyronine
-Calcitonin

36
Q

Describe mechanism of action of thyroxine and tri-iodothyronine

A

Metabolic
-Increased basal metabolic rate
-Increased protein catabolism
-Increased glycogenolysis

Cardiac
-Increased heart rate (increased sensitivity of beta receptors to catecholamines)
-Increased cardiac output

CNS:
-enhances sympathetic activity
-Aids development of CNS

GI:
-Increased glucose absorption from GI tract
-Increased GI motility
-Increased GI secretions

37
Q

Describe mechanism of action of calcitonin

A

Inhibits calcium release from bone when serum calcium is high

38
Q

Where is calcitonin produced?

A

Parafollicular C cells of thyroid

39
Q

Which type of thyroid ca produces calcitonin?

A

Medullary thyroid carcinoma

40
Q

Where is TSH released from?

A

Anterior pituitary

41
Q

Where is TRH released from? What is its function?

A

-Hypothalamus
-TRH stimulates anterior pituitary to release thyroid stimulating hormone and prolactin

42
Q

How are thyroid hormones synthesised?

A

-Iodide absorbed into follicular cell–> iodine by thyroid peroxidase
-Iodine + thyroglobulin out, combined with tyrosine–> iodotyrosine or diiodotyrosine
-iodotyrosine/diiodotyosine in: T3 and T4 out

-Iodide is absorbed form plasma into thyroid follicular cell where it is converted to iodine by thyroid peroxidase
-Iodine secreted from thyroid follicular cell with thyroglobulin is combined with tyrosine to form iodotyrosine or di-iodotyrosine
-Iodotyrosine/di-iodotyrosine is transported back into thyroid follicular cell
-Two di-iodotyrosines or one di-iodotyrosine and one iodotyrosine to form T3 and T4 respectively
-T3 and T4 are secreted into bloodstream and transported bound to proteins

MRCS Critical care (11 decks)

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