Brainscape's Knowledge GenomeTM

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


See full index

Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

How is T3 and T4 released stimulated

A
  • thyrotrophin releasing hormone from hypothal
  • TSH anterio rpituitary
  • T4, T3 thyroid
  • negative feedback to hypothalamus (less TRH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do T3 and T4 bind to after release to be transported

A

thyroxine binding globulin and albumin

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

how do T3 and T4 become activated

A
  • T3 is active on release

- T4 is activated peripherally by losing an iodine molecule

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

what are the function of thyroid hormones and what receptors do they stimulate

A
  • increase metabolism
  • via nuclear receptors
  • growth and mental development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What states are thyroid binding globulin increased/reduce din

A

Increased:

  • pregnant
  • oestrogen therapy
  • hepatitis

Decreased- low protein states

  • nephrotic syndrome
  • chronic liver disease
  • acromegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does primary hyper/hypothyroidism mean

A
  • problem with the thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TFT results for primary hyperthyroid

A

low TSH, high T4

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

TFT results for primary hypothyroid

A

hihg TSH , low T4

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

what does central hypo/hyperthyroid mean

A

issue with pituitary or hypothalamus

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

sx of hyperthyroid

A 
Sweating
Weight loss
****Emotional lability (irritable, psychosis)
Appetite increase
Tremor/tachycardia (AF)
Intolerance to heat/irregular menstruation
Nervousness/anxiety
Goitre/GI problems (diarrhoea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

signs for hyperthyroid

A
  • tachycardia/AF (can cause lightheadedness/syncope)
  • ****- palmar erythema
  • goitre
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

most common cause of hyperthyroidism

A

Grave’s

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

Causes of hyperthyroidism

A

Grave’s
toxic multinod. goitre
toxic adenoma (1x nodule)
***ectopic thyroid tissue (mets, ovarian teratoma)

***pituitary adenoma secreting TSH

exogenous-

  • iodine excess
  • levothyroxine excess
  • *****- amiodarone, lithium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

tx of hyperthyriodism

A

carbimazole- TFTs and sx guide dose - titrate

  • ***propylthiouracil (2nd line)
  • ***beta-blockers (AF)

radioiodine
thyroidectomy

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

what are the sx of a thyroid storm

A

life threatening

tachycardia, HTN
anxiety/restlessness
fever (>40)
mental status changed
D+V
\+- jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

tx thyroid storm

A
  • **antithyroid drug- - carbimazole OR propylthiouracil
  • **beta blockers IV
  • **steroids- hydrocortisone or dexamethasone - blocks T4 T3 conversion
  • fluids, NG if vomiting
  • bloods- TFT, cultures
  • BP monitoring
  • tx any infection
  • paracetemol for fever

BB alternatives- diltiazem/verapamil, digoxin (AF)

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

causes of thyroid storm

A

person with thyroid disease and:

  • fever, sepsis
  • dehydration
  • MI
  • radioactive iodine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is grave’s disease

A

hyperthyroidism due to circulating autoantibodies

  • activate TSH receptors
  • also react with orbital autoantigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what genetic mutation is grave’s disease associated with?

what other conditions are also associated with this mutation?

A

HLA-DR3

vitiligo
T1DM
addisons

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

what populaitons is grave’s disease more commonly seen in

A
  • females

- pregnant/post-partum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

sx of Grave’s disease

A

hyperthyroidism- SWEATING

****- pretibial myxedema
- Goitre- smooth thyroid enlargement
eye disease
Ophthalmology
- upper eyelid retraction with lid lag,
- swelling, erythema, conjunctivitis of the eyes
- exophthalmopathy (bulging)
- diplopia
- discomfort, grittiness/tearing

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

what autoantibodies are seen in graves

A
  • thyroid stimulating hormone receptor antibodies- gold standard
  • thyroid perioxidase antibodies (also in Hashimoto’s)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

symptoms of hypothyroid

A

BRADYCARDIC

Bradycardia
Reflexes slow
Ataxia
Dry, thin hair and skin
Yawning (fatigue)
Cold (low temp)
****Ascites and non-pitting oedema
****Round face, obesity
Depression
**Immobile (proximal weakness), ileus
***Congestive HF, constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

causes of hypothyroidism

A 
Iodine deficiency 
Primary atrophic hypothyroid
Hashimoto's thyroiditis
thyroidectomy
drug induced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is primary atrophic thyroiditis

A

diffuse lymphocytic infiltration of thyroid
leads to atrophy
no goitre
no autoantibodies

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

tx of hypothyroidism

A

levothyroxine

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

what is autoimmune/hashimoto’s thyroiditis

A
  • lymphocytic and plasma infiltration
  • goitre
  • autoantibodies
  • assoc with other AI conditions and MALT lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

autoantibodies found in hashimotos/autoimmune thyroiditis

A

*****thyroglobin antibodies

thyroid peroxidase antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is myxoedema coma, sx

A
  • severe hypothyroid state, precedes death
  • hypothermia
  • hyporeflexia
  • low glucose
  • bradycardia
  • coma, seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what can cause myxoedema coma

A
  • infection
  • MI
  • stroke
  • Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

management myxoedema coma

A
  • ****- TFT, FBC, UE, cortisol, glucose, cultures
  • ****- ABG
  • active warming
  • **- correct hypoglycaemia
  • **- tx infection
  • IV T3 (Liothyronine) very slowly, sometimes can give levothyroxine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is postpartum thyroiditis

A

hyper/hypothyroisism within the first year following a birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is foetal thyrotoxicosis, what can it cause

A

when TSH- receptor antibodies (Graves) cross the placenta

- can cause cardiac conditions, IUGR, foetal goitre, hydrops, preterm, miscarriage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

management of foetal thyrotoxicosis

A
  • anti thyroid meds- carbimazole to mother
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is gestational thyrotoxicosis

A
  • 1st 1/2 of pregnancy

- T4 raised, low TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

tx of gestational thyrotoxicosis

A
  • propanolol
  • carbimazole
  • surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

mots common type of thyroid cancer

A

papillary- good prognosis

Paul’s Focaccia Most Awarded Loaf- papillary>follicular>medullary>anaplastic>lymphoma

-anaplastic- v bad prog

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ix for ?thyroid cancer

A

aspirate large nodule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

tx thyroid cancer

A

hemi/total thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

complications of thyroidectomy

A
  • external superior laryngeal- voice change, loss of high pitch
  • recurrent laryngeal- hoarse, weak voice
  • BL recurrent laryngeal- lose voice, need tracheostomy
  • hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are the 2 tyes of cells in the parathyroid glands

A 
chief cells
oxyphil cells (unknown use)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what do chief cells secrete

A

PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what does PTH do

A

released when Ca levels low
- increases serum Ca

  • increased bone resorption
  • increased Ca re-absorption in kidneys
  • Vit D synthesis- which then acts on the gut to increase Ca absorption
  • negative feedback- Ca=less PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

causes of primary hyperparathyroidism

A
  • solitary adenoma
  • general hyperplasia
  • cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

sx hyperparathyroidism

A 
Bones- pain, #, OP
Stones
Groans- abdo pain, constipation
Moans- confusion, delirium, agitation, depression
Thrones- polydipsia, polyuria

pancreatitis
weakness
fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

blood resuts in primary hyperparathyroidism

A
  • hgih Ca
  • PTH high
  • reduced phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is secondary hyperparathyroidism

A

high PTH, but being released in an appropriate response to consistently low Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

causes of secondary hyperparathyroidism

A
  • low vit D
  • chronic renal failure (increased Ca excretion)
  • low Ca intake
  • reduced intestinal Ca absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

tx primary hyperparathyroidism

A
  • fluids
  • high Ca and vit D intake
  • excise adenoma/PT glands
  • conservative- cinacalcet- calcimimetic- increases PT cell sensitvity to Ca to increase -ve feedback- if surgery is unsuccessful
  • consider bisphos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

tx secondary hyperparathyroidsm

A
  • correct cause
  • phosphate binders
  • Vit D
  • cinacalcet - a calcimimetic- increases PT sensitivity to Ca
  • parathyroidectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

blood results in secondary hyperparathyroidism

A

low Ca

high PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is tertiary hyperparathyroidism

A
  • very LT secondary hyperparathyroidism
  • hyperplasia
  • inapp. PTH desensitised to Ca serum levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

blood results for tertiary hyperparathyroidism

A
  • high Ca, very high PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is primary hypoparathyroidism

A

failure of the glands- low PTH excretion leading to low Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

causes of primary hypoparathyroidism

A

autoimmune destruction

  • type 1- AIRE mutations
  • Type 2- HLA D3+ and HLA D4

congenital eg diGeorge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

test results for primary hypoparathyroidism

A

low PTH, low Ca

high or normal phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

sx of hypoparathyroidism

A 
- petechiae/purpura
tingling around mouth 
tetany 
muscle spasms
seizures
confusion
cardiac arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

tx primary hypoparathyroidism

A

calcium
calcitriol
synthetic PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is and what causes secondary hypoparathyroidism

A

high calcium level

  • malignancy- bony mets, vit D secretion of lymphoma, myeloma, lung, breast
  • rapid burn turnover
  • renal failure
  • thiazides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is pseudohypoparathyroidism

A
  • failure of target cells to reposond to PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

SIGNS of pseudohypoparathyroidism

A
  • short metacarpals
  • short stature
  • round face
  • calcified basal ganglia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

test results for pseusohypoparathyroidism

A
  • low Ca
  • high PTH
  • hgih phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

tx pseudohypoparathyroidism

A

Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the zones of the adrenal cortex

A

Glomerulosa
Fasiculata
Reticularia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what does the glomerulosa of the adrenal cortex, produce?

A

mineralocorticoids

- aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what stimulates the glomerulosa of the adrenals

A
  • kidneys produce renin (low BP)
  • angiotensin, thats produced from liver, converted to angiotensin I
  • ACEI (lungs) cnoverts angiotensin I to angiotensin II
  • aldosterone production from adrenals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what does aldosterone do

A
  • increases BP
  • increases Na and H2O retention
  • increases K excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what does the fasiculata of the adrenal cortex, produce?

A
  • glucocorticoids

eg cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what is the function of cortisol

A
  • increase glucose in blood

- increases gluconeogenesis in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

how is cortisol release stimulated

A

HPA axis

  • hypothal produces corticotrop. releasing hormone
  • ant pit produces adrenocorticotropic hormones
  • adrenals release cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what does the reticularis zone of the adrenal cortex secrete

A

androgens (testosterone precursors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how is androgen release from adrenals stimulated?

A

HPA axis- CRH hypothal–> ACTH from ant. pituitary–> stimulation of adrenal cortex zona reticularis to prod. androgens (testosterone and others)

ACTH also stimulated cortisol release from adrenals, and to a much lesser extent , aldosterone

NB- production of testosterone does not rely on 21-hydroxylase, yet cortisol and aldosterone does (relevant in CAH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what part of the adrenal glands are responsible for the production of catecholamines eg noradrenaline, adrenaline

A

medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

when are catecholamines stimulated to be secreted

A

Adrenaline, norepinephrine, dopamine

Sympathetic innervation

Adrenergic receptors

  • alpha (arteries)
  • beta-1 (heart- increase HR, contractility)
  • beta-2 (bronchioles and arteries of the skeletal muscles)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what is Cushing’s syndrome

A

clincial state produced by chronic glucocorticoid excess and loss of normal feedback mechanisms of HPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is primary Cushing’s syndrome

A

non-ACTH dependent:

  • issues with adrenal gland
  • increased release of steroid hormones without stimulation by HPA axis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

blood results of primary Cushing’s syndrome

A
  • *cortisol-secreting adenoma in the cortex of the adrenal gland**
  • low ACTH (release is activated by CRH)
  • high cortisol
  • ACTH suppression test will not affect amount of steroid in blood, but suppresses ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

causes of primary Cushing’s syndrome

A
  • adrenal adenoma/cancer

- adrenal nodular hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is secondary Cushing’s syndrome

A

increased ACTH

causing high steroid serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

causes of secondary Cushing’s syndrome

A
  • Cushing’s disease (ACTH secreting pituitary tumour)

- Ectopic ACTH- SCC, carcinoid tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

sx of Cushing syndrome

A
  • increased weight (central)
  • mood change (depression, psychosis, irritability)
  • skin, muscle atrophy
  • gonadal dysfunction (irregular menses, hirtuisism, ED)
  • acne
  • moon face
  • bufalo bump
  • easy bruising
  • purple abdo striae
  • OP
  • HTN
  • hyperglycaemia
  • poor healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

sx of Cushing’s disease/pituitary tumour

A
  • Cushing’s syndrome
  • bitemporal hemianopia
  • headaches
  • CN III, IV, VI palsy (eye movements)
  • diabetes insipidus (low ADH)- tumour pushes on post. pituitary
  • temp/sleep/appetite control issues
  • CSF leak through nose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what skin changes occur in very high levels of ACTH

A
  • yellow/tanned

seen in ectopic ACTH production and addisons (increased ACTH in response to low adrenal activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

ix for Cushing’s syndrome

A
  • plasma cortisol (raised)
  • 24hour urinary free cortisol
  • midnight cortisol levels
  • plasma ACTH
    **- low dose dexa methasone suppression test- 1mg
    Normal– dexa- hypothal CRH reduced, ACTH from pituitary reduced , cortisol level supressed
    Abnormal- cortisol level not supressed

High dose dex supp (8mg)

  • pit adenoma- Cort and ACTH suppressed
  • Adrenal adenoma- cortisol not supressed, ACTH suppressed
  • Ectopic ACTH - both not suppressed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

tx of Cushing’s syndrome

A
  • **Metyrapone- reduce cortisol prod.
  • **Ketoconazole - reduce cortisol prod.

Adrenal adenoma/carcinoma (primary):
- adrenalectomy

Paraneoplastic/Cushing’s disease (secondary)

  • surgery - removal of tumour
  • RT

Iatrogenic
- stop steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is Addison’s

A

Primary adrenal Insufficiency

No negaive feedback to pituitary or hypothal (high ACTH levels, low cortisol/aldotserone/androgens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

sx of addison’s

A
  • GI- abdo pain/diarrhoea/constipation
  • weakness, fatigue
  • weight loss
  • hyperpigmentation of skin (golden)/vitiligo- high ACTH released from ant. pituitary
  • depression, psychosis, low self esteem
  • hyponatraemia- N+V, headache, fatigue, weakness/cramps/spasms, confusion, seizures, coma
  • hyperkalaemia- abdo pain, diarrhoea, palpitations, weakness, paraesthesia, N+V
  • hypercalcaemia- stones, moans, groans, thrones, polyuria/polydipsia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

causes of Addisons’

A

primary

  • destruction of adrenals
  • autoimmune
  • **- infective (TB, CMV, HIV)
  • adrenal haemorrhage
  • malignancy
  • **Secondary
  • LT steroid use supresses pituitary ACTH production, so adrenals underproduce steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

ix for ?addison’s

A
  • low Na and high K- low mineralocorticoids (aldosterone)
  • low glucose (low cortisol)

-uraemia, hyperCa, eosinophilia, anaemia

  • ACTH response test- cortisol response to ACTH measured- no response in primary/LT secondary
  • ACTH- high in primary addison’s , low in secondary causes
  • 21-hydroxylase autoantibodies for autoimmune (primary) cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

tx addisons

A
  • stop exogenous corticosteroid slowly if possible
  • hydocortisone (cortisol and mineralocorticoid action)
    +- fludrocortisone (mineralocorticoid, replaces aldosterone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what is primary hyperaldosternoism

A

Conn’s
excess production of aldosterone, independent of RAAS

Cause:

  • adrenal adenomas
  • adrenal hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what is seondary hyperaldosteronism

A

ecxess aldosterone due to hgih levels of renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

ix for primary hyperaldosteronism (Conn’s)

A
  • aldosterone-to-renin ratio- high (ald high, renin levels low)- GOLD STANDARD
  • UEs- low K, high HCO3, high Na
  • CT abdo- adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what is Conn’s syndrome

A
  • primary hyperaldosteronism

Causes:

  • solitary aldosterone producing adrenal adenoma
  • adrenal gland hyperplasia
  • adrenal cancer
  • familial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

causes of secondary hyperaldosteronism

A 
***Due to excessive RAAS activation****
renal artery stenosis
accelerated HTN
diuretics
cong HF
hepatic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is Batter’s syndrome

A
  • loss of Na and Cl in loop of henle (defect channels)
  • sodium loss means volume depletion
  • increased renin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

sx of hyperaldosteronism

A

asx

Hypernatraemia:

  • weakness
  • polydipsia, thirst
  • confusion

hypokalaemia:

  • paraesthsia
  • cramps, weakness, paralysis
  • polyuria
  • polydipsia
  • HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

tx of hyperaldosteronism

A
  • Conn’s- removal of adenoma
  • aldosterone antag- spironolactone, eplerenone
  • *- dexamethasone (supresses aldosterone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

where is prolactin produced

A

anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what inhibits prolactin secretion

A

dopamine form hypothal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what substances does the posterior pituitary secrete

A

ADH

  • made inhypothal, stored in post, pit
  • increase water reabs– increases osmolality of the urine
  • aquaporin 2 in DCT

oxytocin-

  • milk
  • behaviour
  • myometrial contraction
102
Q

Whhat does the hypothal produce? what does this then stimulate production form ant.pit–> what do these then cause the production of?

A
  • TRH–>TSH –> T3/4
  • CRH–>ACTH –> cortisol (adrenal zona fasciculata)
  • GnRH–> LH/FSH
  • dopamine –X-> prolactin (lactotroph cells)
  • GHRH–> GH
103
Q

causes of hypopituitarism

A

HYPOTHAL

  • Kallmans (ansomnia, GnRH X)
  • tumour
  • inflammation
  • infection
  • ischaemia

PItuitary

  • trauma, surgery, radiation
  • tumour, mass, meningoma , mets
  • carotid artery aneurysm
  • ischaemia- eg Sheehans, DIC
  • haemochromatoisis, amyloid
  • inflammation
  • autoimmunity
104
Q

sx and signs of hypopituitarism

A

TSH
- BRADYCARDIA

GH

  • obesity
  • atheroscerosis
  • dry skin
  • weakness, loss of balance
  • low CO

FSH, LH
- oligo/amenorrhoea, ED, OP

ACTH

  • adrenal insuff/addison’s- GI, wt loss, weakness, low mood, confusion, hypotension, electrolytes
  • no skin pigment changes

ADH

  • polyuria
  • polydipsia
  • electrlyte
105
Q

tx of hypopituitarism

A
  • hydrocortisone (low ACTH- aldosterone and cortisol replacement)
  • thyroxine- (low TSH)
  • testosterone/oestrogen (low FSH/LH)
  • **- somatotrophin (mimics GH)
106
Q

tx of prolactinoma in pituitary

A

dopamine agonist (bromocriptine)

  • OP prevention
  • surgery- to remove tumour
107
Q

what is pituitary apoplexy

A

rapid pituitary haemorrhage due to tumour

  • acute hypopituitarism, cardiac collapse, mass effects, death
  • headache, meningism, decreased GCS, LoC
108
Q

tx pituitary apoplexy

A

hydrocortisone IV ( has mineralocorticoid and glucocorticoid actions- mimics aldosterone (and cortisol) and so prevent ssalt losing crisis)
fluid balance
operate

109
Q

Causes of acromegaly

A

pituitary tumour

hyperplasia due to ectopic GHRH from another tumour

110
Q

sx acromegaly

A
  • paraesthesia, carpal tunnel, prox weakness
  • headache, - bitemp hemianopia
  • sweating
  • snoring
  • arthralgia
  • large hands and feet, gigantism
  • diabetes, DKA
  • cardiomegaly, arrhythmias
  • hepatosplenomegaly
  • goitre
  • colon cancer

hypopituitarism-

  • hypothyroid (TSH)
  • polyuria, polydipsia, confusion, low BP (ADH)
  • hypotension, N+V, weakness, wt loss (low ACTH)
  • low libido, amenorrhoea (LH/FSH)
111
Q

ix for acromegaly

A
  • GH- diurnal so NOT helpful
  • glucose, IGF-1, prolactin, cortisol, thyroid, gonadal hormones
  • high Ca, phosphate (high bone turnover)
  • MRI pituitary
  • visual field testing
  • ECG
  • ECHO (cardiomegaly)
  • CT- lung, pancreas, adrenals, ovaries- ectopic GH release
112
Q

tx acromegaly

A
  • somatostatin analogues- oppose GH eg OCREOTIDE
  • GH antagonist- PEGVISOMANT
  • remove pit tumour
  • radiotherapy if large
113
Q

what is diabetes insipidus

A
  • reduced ADH /vassopressin secretion from post. pit or low response to ADH in kidneys
  • impaired water resorption
114
Q

sx diabetes insipidus

A

polyuria
polydipsia
- hypernatraemia- as ADH causes water resorption without assoc electrolyte reabs– concentrated Na due to water loss— lethargy, weakness, irritable, myoclonic jerk, seizures

115
Q

ix diabetes inspidus

A
  • UE, Ca, Na
  • Glucose- r/o DM
  • urine and plasma osmolalities- high in plasma (drinking alot of water), low in urine (dilute urine)
  • fluid deprivation test if diagnosis reminas unclear (no fluids for 4-12hours- no change in the water loss)
  • desmopressin stimulation test- to distinguish between the two types of diabetes insipidus (central- would reduce water loss- nephrogenic- no change in water loss)
116
Q

tx diabete insipidus

A
  • tx cause (cranial/nephrogenic)
  • reduce Na with 0.9% saline at a rate of <12mmol/L/day
  • desmopressin IM (man made ADH)– will help if central cause to DI, if nephrogenic cause, wont help
117
Q

what is SIADH

A

syndrome of inappropriate ADH

118
Q

sx SIADH

A
  • hyponatraemia- anorexia, nausea, malasia, low GCS, headache, irritability
119
Q

causes of SIADH

A
  • paraneoplastic tumours secreting ADH- SSC, pancreas, prostate, thymus, lymphomas
  • CNS issues
  • chest- TB , pneumonia, abscess
  • thiazide like diuretics, carbamazepine, NSAIDs, opiates, SSRIs
120
Q

ix results in SIADH

A
  • hyponatraemia (diluted blood)

- highly concentrated urine (high osmolality)

121
Q

tx SIADH

A

tx cause
restrict fluids
salt
loop diuretics if severe

122
Q

what are cacinoid tumours

A

slow growing neuroendocrine tumours
secrete neuropeptides- serotonin, histamine and postaglandins
appendix, small intestine

123
Q

tx carcinoid tumours

A

***ocreotide (somatostatin analogue- inhibits the secretion of other hormones)
resection

124
Q

what is multiple endocrine neoplasia

A

group of genetic conditions
growth of hormone producing tumours in endocrine organs

MEN 1- 3ps

  • parathyroid
  • pancreas
  • pituitary
MEN 2
A
- medullary thyroid
- Pheochromocytoma
- parathyroid hypeprlasia
B
- medullary thyroid
- Pheochromocytoma
- Marfans/neuromas
FMTC- Familial Medullary Thyroid Carcinoma- medullary thyroid Ca is only feature
125
Q

what is a phaeochromocytoma, sx

A

catcecholamine (adrenaline) producing tumours

sx

  • anxiety
  • sweating
  • HTN (crisis= cardiogenic shock)
  • palpitations, tachy, AF
  • headache
126
Q

how do you tx HTN crisis that may occur due to phaeochromocytoma

A
  • IV alpha blcoker- phentolamine
  • then long acting one- phenoxybenzemine
  • beta blocker
  • surgery on tumour once controlled
127
Q

What does LH do in males

A

stimulate Leydig cells to produce testosterone

- negative feedback on hypothal GnRH and ant. pituitary LH production

128
Q

What does FSH do in males

A

stimulate Sertoli cells to produce androgen binding globulin and inhibin
- inhibin has negative feedback effect on hypothal GnRH and ant. pit. gland

129
Q

What effect does FSH and LH have on the female ovaries

A
  • produce oestrogen and follicular development
  • when oestrogen levels peak- FSH inhibited and LH surges
  • progesterone prod. by corpus luteum inhibits LH secretion
130
Q

what is the definition of precocious puberty

A
  • breast development <8
  • testicular enlargement >3-4ml <9
  • more common in girls, more worrying in boys
131
Q

causes of precocious puberty

A

True/central

  • gonadotrophin dependent
  • FSH and LH raised
  • congenital or hypothalamic tumours

Pseudo

  • gonadotrophin independent
  • FSH and LH low
  • adrenal (tumour, Cushing’s, CAH)- build up of precursors
  • gonadal- tumour, cyst
  • exogenous steroids
132
Q

A 7 year old boy presents with his mother. His mother complains he is already developing secondary sexual characteristics. O/E testicular volume is 4ml. What red flag symptoms should you ask about

A

Central cause (tumour)- hydrocephalus

  • headhaches
  • changes in vision
  • changes in eye movements
  • drowsiness
  • N+V
  • poor balance and coordination
  • seizures
133
Q

ix for precocious puberty

A
  • LH, FSH, estradiol and testosterone

If LH/FSH high (central)

  • MRI head
  • tumour markers- bHCG, AFP

if LH/FSH low (pseudo)

  • adrenals- abdo imaging, urine steroid
  • gonadal imaging
134
Q

tx precocious puberty

A
  • radiation
  • chemo
  • surgery
  • steroids for hydrocephalus
135
Q

definition of late puberty

A
  • no breast development by 13yo
  • testicles <4ml in boys by age 14
  • more common in boys
136
Q

causes of late puberty

A

Intact hypothalamo-pituitary axis

  • consitutional
  • chronic illness
  • excessive sport
  • psychosocial deprivation
  • steroids

Impaired hypothal-pit axis (hypogonadotrophic hypogonadism)

Peripheral- hypergonadotrophic hypogonadism

137
Q

name some causes of hypogonadotrophic hypogonadism

A
  • intracranial tumours
  • congenital- Kallman’s
  • irradiation
  • trauma- head injury, surgery
  • sheehans
138
Q

name some causes of hypergonadotrophic hypogonadism in boys

A
  • BL testicular damage- cryptorchidism, atresia, torsion, infection (mumps), failed orchidoplexy
  • **- conditions that cause crytorchidism/gonadal dysgensesis eg Noonan’s, prader-willi- klinefelters XXY
  • ***- inborn steroids enzyme deficiencies
  • damage- surgery, chemo, RT, trauma, autoimmune
139
Q

name some causes of hypergonadotrophic hypogonadism in girls

A
  • dysgenesis- tuner’s, prader-willi
  • drugs- cyclophosphamide
  • intersex- androgen insensitivity, CAH
  • inborn steroid enzyme deficiencies
  • PCOS
    premature failure
  • toxicity- galactosaemia (inherited, galactose), thalassaemia (iron)
  • damage- surgery, CT, RT, trauma, autoimmune
140
Q

ix for late puberty

A
  • FBC (anaemia), ferritin, UE, coeliac screen, urinanalysis, TFT, bone profile
  • bone age- central, hypothyroidism, GH deficiency
  • FSH, LH
  • Prolactin, insuline like GF
  • chromosomal testing
  • Girls- pelvis USS

If hgih FSH/LH (peripheral, hypergonadotrophic cause)

  • sex chromosome testing
  • HCG testing
  • sweat sodium testing

Low FSH/LH (central, hypogonadotrophic cause)

  • MRI head is sx
  • screen for chronic illnesses
  • GH, cortisol testing for pituitary functioning
  • karyotype
  • constitutional?
141
Q

tx for late puberty

A
  • oral oxandrolone
  • low dose IM testosterone in boys
  • oestradiol in girls
  • tx underlying cnodition if necessary
  • remove tumours/chemo/RT
142
Q

definition of arrested puberty

A
  • lack of pubertal progression for >2years after spontaneous onset at appropriate age
143
Q

common presenting issues with arrested puberty

A
  • failure to achieve menarche and thelarche (start then stop)
  • failure to reach >15ml tetsicular size from 4ml for >5years
  • poor breast development
  • suboptimal growth spurt
  • poor male virilisation (bulk, deep voice, hair)
144
Q

management of arrested puberty

A
  • pathological until proven otherwise

- urgent referral and ix

145
Q

Pathophysiology of PCOS

A
  • hyperinsulinaemia due to insulin resistance
  • causes increased androgen production (theca cells in ovaries)
  • reduced available sexhormone binding globulin by liver– free testosterone raised
146
Q

what is the name of the criteria used for PCOS

A

Rotterdam

147
Q

What is the rotterdam criteria

A

2 of the following

  • oligo/anovulation/amenorrhoea
  • hyperandrogenism (clinically or biochemically)- exclude renal cause
  • polycystic ovaries on USS
148
Q

sx of high testosterone in females

A

hirtuism
male pattern alopecia
- increased muscle mass, deep voice if severe

149
Q

other sx of PCOS not included in rotterdam criteria

A
  • infertility/subfertility
  • acne
  • mood swings, depression, anxiety, low self-esteem
  • sleep apnoea, obesity
  • acanthosis nigrans- insluin resistance
  • painful iliac fossa if cysts are large (unsual)
150
Q

ddx for hirtuism/high androgen sx

A

hyperandorgenism:

  • PCOS
  • CAH
  • androgen secreting tumours (adrenal, ovarian)
  • androgen therapy
  • Cushing’s
  • Thyroid dysfunction
  • hyperprolactinoma
  • SE of meds- phenytoin, corticosteroids
  • obesity (increased insulin resistance)
151
Q

ix for ?PCOS

A
  • total testosterone and free testosterone
  • USS ovaries
  • *- sex hormone binding globulin- normal/low
  • *- LH- may be elevated, LH:FSH ratio increased
  • fasting glucose tolerance test- insulin resistance
  • asses CV risk and lipid levels

R/o other causes of hyperandrogenism

  • TFT
  • 17-hydroxyprogesterone levels (CAH)
  • prolactin
  • 24hr urinary cortisol
152
Q

tx PCOS

A
  • weight <30 BMI
  • COCP , cyclical progesterone
  • IUS

Clomiphene or tamoxifen

  • For fertility , anti-oestrogen
  • restarts GnRH pulse
  • makes pit produce more FSH as body thinks you have low oestrogen
  • give up to 6x cycles, don’t give >12m as risk of ovarian Ca

Metformin- less effective, esp if obese, may help if clomiphene resistant, GI SE

  • Laparoscopic ovarian drilling
  • Gonadotrophin ovulation induction (gonadotrophin injections)
  • Assisted conception tx
153
Q

sx of prolactinoma

A
  • menstrual dysfunction - amenorrhoea, oligomenorrhoea, anolvulation
  • delayed puberty, growth failure
  • infertility, reduced libido
  • galactorrhoea
  • OP
  • tumour- headache, visual changes
  • men - ED, reduced hair growth , gynaecomastia
154
Q

blood tests in prolactinoma

A
  • high prolactin

* *- low GnRH, FSH, LH (negative feedback on hypothal and ant pit)

155
Q

ix ?prolactinoma

A
  • TFTs
  • pregnancy tets
  • serum prolactin, GnRH, FSH, LH
  • visual field testing
  • MRI head
156
Q

causes of azoospermia

A
  • can be primary (hypergonadotrophic) or secondary (hypogonadotrophic)

Hypogonadotrophic (primary):

  • chemo/RT
  • idiopathic
  • genetic

Hypergonadotrophic (secondary):
- obstructive- varioceles, epididymis obstruction, previous inguinal/scrotial injury, hernia repair, vasectomy

157
Q

what is retrograde ejaculation

A
  • semen passes into bladder rather than along urethra
158
Q

causes of retrograde ejaculation

A
  • transurethral resections of the prostate
  • bladder neck incisions
  • *- psychotrophic meds
  • *- alpha adrenergic blockers- doxazosin, prazosin (HTN, BPH)– smooth muscle/sphincter relaxation
  • *- spinal cord lesions
  • congenital anatomical cause
159
Q

sx of retrograde ejaculation

A
  • abscence of ejaculate

- cloudy urine post-organsm

160
Q

ix ?retrograde ejac

A
  • post ejaculatory urine - spermatozoa, seminal fluid, or fructose
161
Q

tx of retrograde ejac

A
  • alpha adrenergic agonists (clonidine)- sympathomimeitc, smooth muscle and BV constriction
  • antihistamines
162
Q

WHO classification of female infertility

A

I

  • hypothalamic /pituitary/hypognoadism
  • pit tumour
  • sheehans
  • stress, wt loss, exercise
  • hyperprolactinoma

II- normogonadotrophic– PCOS

III- ovarian failure/hypergonadotrophic

  • premature menopause
  • chromosomal disorder
  • surgery, trauma, RT
163
Q

What level counts as hypocalcaemia

A

<2.1mmol/L

164
Q

Causes of hypocalcaemia

A
  • low vit D/Ca intake/malabs
  • hypoparathyroidism (post thyroidectomy, idiopathic, diGeorge, infiltration)
  • meds- bisphos, cisplatin, loop diuretics
  • CKD/chronic liver disease
  • AKI, rhabdomyolysis
  • acute pancreatiits
  • **- hungry bone syndrome post parathyroidectomy- assoc with hypophosphataemia and hypoMg, exacerbated by supressed PTH levels following parathyroidectomy
  • osteomalacia
  • tumour lysis syndrome
165
Q

Presentation and signs of hypocalcaemia

A
  • paraesthesia
  • tetany/fasciulations
  • myoclonic jerks
  • seizures/convulsions
  • chronic- dementia/confusion
  • Chvostek’s VII CN sign
  • Trousseau sign- BP cuff to 20mmHg for 5 mins
166
Q

tx hypocalcaemia

A

Acute/severe/sx
- 10ml 10% Ca gluconate IV in 10min, slow infusion after

Chronic
- Vit D 1.25-2.5mg per day
- Ca 600mg per day
ie Adcal 1500mg (Ca 600mg), sandocal (Ca 1g)

167
Q

ix hypocalcaemia

A
  • ECG- long QT
  • PTH
  • Vit D
  • amylase
168
Q

what level is hypercalcaemia

A

> 2.6mmol/L

169
Q

causes of hypercalcaemia

A
  • hyperparathyroidism
  • malignancy- bone mets, myeloma, lymphoma
  • **sarcoidosis
  • paget’s
  • meds- thiazide like diuretics, lithium**, Ca
  • *****thyrotoxicosis
  • *****addisons, phaeochromocytoma
  • false- sample kept too long/too hot
170
Q

ix hypercalacemia

A

ECG- short QTc

  • vit D
  • PTH
  • XR- cancer
  • Ig - serum (monoclonal bands) , urine (bence jones)
171
Q

sx hypercalcaemia

A
  • Stones
  • Moans (psych)
  • Groans (abdo pain, N+V)
    Thrones- constipation, polyuria
  • polydipsia
172
Q

tx hypercalcaemia

A
  • cause
  • bisphosponates IV - zolendonate
  • Saline
  • Ph, Mg
173
Q

level of hypernatraemia

A

> 140mmol/L

174
Q

causes of hypernatraemia

A

Extra-renal

  • dehydration- water intake, D+V, sweating/burn
  • excess salt intake
  • too much IV saline

Renal

  • diabetes insipidus (concentrated)
  • ***- Conn’s- hyperaldosteronism (reabs)
  • ***- Cushings- cortisol exhibits minerlocorticoid activity in high conc
  • **- osmotic diuretics, loop, thiazide diuretics, lithium, mannitol
  • pseudo- if taken from site near fluid input
175
Q

sx hypernatraemia

A
  • tired, weak, confusion, irritable
    Nausea
  • thirst, reduced turgor, dry mouth, oliguria, tachycardia, orthostatic hypo
  • muscle twitching, seizure, coma
176
Q

ix hypernraemia

A
  • Ca, glucose, UE

- paired urine and serum osmolarity

177
Q

tx hypernatraemia

A
  • oral rehydration
  • IV hypotonic fluids- 5% dextrose, 0.45% saline slowly
  • Na reduction <10 mmol/L/day, reduce cerebral oedema
  • if in shock, resus with isotonic fluids first
  • dialysis if loss of renal function or Na >170mmolL
178
Q

causes of hyponatraemia

A 
ABCDEFGH
ACEI/antids (SSRIs), antipsychotics
*Brivaracetam (anticonvulsion)
Carbamazepine
*Desmopressin/Diuretics
*Ethosuximide
Furosemide
Gliclazide
Heparin
*NSAIDs
  • polydipsia (psychogenic)
  • adrenal insufficiency (addisons, hypopituitarism)- low aldosterone, low reabs
  • SIADH- dilutional
  • chronic, severe D+V, chronic dehydration
  • ecstasy
  • HF, cirrhosis
  • CKD, AKI, nephrotic syndrome
179
Q

sx of hyponatraemia

A
  • confusion
  • N+V
  • muscle cramps
  • drowsiness
  • seizures
180
Q

ix of hyponatraemia

A
  • UE
  • serum and urine osmolality
  • monitoring ACTH/cortisol (adrenal insufficiency)
181
Q

tx hyponatraemia

A
  • SIADH- fluid restrict
  • hypertonic saline (3%)
  • DEMECLOCYCLINE (ADH agonist)
  • hyervolaemic- loop diuretics
182
Q

serum levels of hypkalaemia

A

> 5.4mmol/L

183
Q

causes of hyperkalaemia

A

**THANKS C
Trimethoprim, Heparin, ACEI/ARBs, NSAIDs, K sparing diuretics, Suxamethonium, Cicocporin

  • AKI/CKD (decreased excretion)
  • addison’s
  • *- increased intake- spinach, TPN, fruits, seweed, nuts
  • *- metabolic acidosis- dehydration, sepsis
  • *- insulin deficiency- moves K into cells (DKA)
  • rhabdomyolysis/tumour lysis syndrome- cell breakdown
  • iatrogenic- blood transfusions
  • *- rewarming after hypothermia
  • pseudo- haemolysis of sample- suspect if in isolation (no kidney strain, no acidosis) and pt is clinically stable
184
Q

sx of hyperkalaemia

A
  • ECG changes (asx)
  • fatigue
  • arrhythmia- palpitations, light-headedness, chest pain
  • paraesthesia
  • flaccid muscle–> paralysis
  • reduced reflexes
  • GI sx- diarrhoea N+V, abdo pain
185
Q

ix hyperkalaemia

A
  • UE- cr, urea, eGFR
  • Ca and CK- rhabdomyolysis
  • blood gas for acidosis
  • ECG
  • med review
186
Q

ECG changes in hyperkalaemia

A
  • tall tented T waves
  • prolonged PR interval, p wave flattening
  • Wide QRS/bizzare qrs morphology
  • bradycardias, bradyarhythmias
  • VT
187
Q

management of hyperkalaemia

A
  • stop K sparring drugs
    1. IV 10% Ca gluconate or Cl if ECG changes present
    2. Insulin up to 10 units with glucose 10%
    3. K binders- Ca resonium, Veltassa
  • salbutamol nebs
  • loop diuretic- increase excretion
  • sodium bicarb infusion- if acidotic
  • dialysis
188
Q

level of hypokalaemia

A

<3.5mmol/L

189
Q

causes of hypokalaemia

A

Urinary loss

  • autoimmune renal issues- SLE, Sjogrens
  • *- renal tubular necrosis
  • diuretics- thiazide, loop
  • *- hypomagnesia- Mg inhibis K excretion, low levels results in increase K excretion

RAAS

  • hyperaldosteronism/Conn’s- K excretion
  • *- renal artery stenosis- RAAS activation
  • *- Cushings- cortisol acts as mineralocorticoid in hgih levels- K excretion
  • *- D+V, laxative abuse
  • *- excess sweating, burns
  • decreased intake
  • *- insulin and glucose tx (into cells)
  • alkalosis
  • other dx- adrenaline, dopamine, salbutamol, CCBs, chloroquine and digoxin intoxication
  • *- hypothermia
  • *- CF
190
Q

sx hypokalaemia

A
  • weakness/paralysis, hypotonia, areflexia, cramps, rhabdomyolysis, myalgia
  • tetany, fasciulation
  • paraesthesia hands/feet
  • fatigue
  • ## constipation–> paralytic ileus (N+V, abdo distension)
191
Q

ix hypokalaemia

A
  • UE< Mg, Ca, Ph, gluc
  • ABG
  • urine K, urine osmolality
  • ECG
  • serum digoxin
  • low dose dexamethasone supression (Cushing’s)
  • pituitary imaging (cushing’s)
  • CT adrenals (conns)
  • renal angiogram- renal artery stenosis, RAAS)
192
Q

Management of hypokalaemia

A
  • cause
  • oral K (sando-K)
  • IV K+ slowly <10mmol/hour
  • replace Mg2+ if needed
193
Q

What may cause a high serum glucose

A

PANC

  • diabetes mellitus
  • acute or chronic pancreatitis
  • *- infiltration of pancreas- haemochromatosis , amyloidosis
  • *- CF
  • pancreatic neoplasia

OTHER ENDO COND.

  • *- Acromegaly (insulin res)
  • Cushing’s- Insulin res
  • Pheochromocytoma- catelcholamine excess, gluconeogenesis, decreased gluc uptake
  • *- hypothyroidism

DRUGS

  • glucocorticoids
  • antipsychotics
  • *- thiazide like diuretics
  • *- protease inhibitors (HIV meds)

STRESSORS- MI, sepsis

194
Q

Cause of diabetes mellitus 1

A

destruction of the beta cells in the iselts of Langerhans

195
Q

diagnostic criteria for diabetes 1

A

sx plus random glucose >11mmol/l, fasting >7mmol/L

no sx + GTT (75g glucose) fasting >7mmol/l or 2hr value >11mol/L

196
Q

sx of diabetes type 1

A
  • polydipsia
  • plyuria
  • blurred vision
  • wt loss and fatigue
  • immunosupression- pruritis vulvulae, balanitis (candidiasis), chest infection
197
Q

genetic link with diabetes mellitus

A

90% have HLA DR3/4

198
Q

management of diabetes type 1

A

education- CHO intake, glucose lowering effect of exercise, LT risks
- test QDS, aiming for fasting level of 5-7mmol/L

Insulin

  • quick acting- (novorapid, humalog), give immediately before (up to 15mins before) meal
  • short acting- actarapid, humulin S- injected 20min before meal
  • Medium actin- humulin I and insulatard- OD/BD
  • Longacting- lantus, levemir- OD usually at bedtime

Regime:

  • Basal bolus regime- short acting before meal, with BD long acting
  • insulin pump- contains short acting insulin only, rate altered depending on glucose levels- if gets disconnected can get hypo and DKA quickly
  • Dose adjustment for normal eating course for pts- reduces DKA and severe hypos
199
Q

insluin to CHO ratio, correction of blood glucose for every insulin unit

A

1 unit for every 15g

1unit brings blood glucose down by 8

200
Q

ix for ?diabetes I

A

bloods- fasting gluc, HbA1c
urinanalysis- glycosuria, ketones
antibodies- anti-GAD, pancreatic islet cell antibody, islet antigen-2 antibody, ZNT8

201
Q

pathophysio of diabetes II

A
  • insulin tolerance and resistance

- some decreased secretion

202
Q

sx diabetes II

A
  • asx
  • gradual fatigue
  • polyuria, polydipsia
  • complications- eg neuropathy, retinopathy
203
Q

Management of diabetes II

A
  • lifestyle
    1. Metformin
    2. Sulphonylureas- gliclazide
  • Thiazoldinediones- pioglitazine
  • DPP-4 inhibitors ‘-liptin’
  • SGLT2 inhibitors ‘-flozin’
  • glucagon-like peptide - 1 analogs- ‘-tide’
  • insulin therapy
204
Q

SE of metformin

A

GI upset
weakness
metallic taste in mouth

dont give if kidney function is poor (lactic acidosis risk)

205
Q

example and SEs of sulphonylureas

A

Gliclazide

  • hypoglycaemia!!!!!- sweaty, hot , confused
  • weight GAIN
  • dont give to older people
206
Q

exmaple and SE of thiazolindinediones

A

pioglitazone

HF!, bladder cancer, wt GAIN, increases sensitivity to insulin

207
Q

example and SE of DPP-4 inhibitors

A

algoliptin

GI, hypos
weight neutral

208
Q

example and SEs and SGLT2 inhibitor

A
  • flozin
    canagliflozin, dapagliflozin, empagliflozin

SE

  • wt loss
  • DKA
  • UTI (glycosuria)
  • necrotising fascitis- advise any pain/erythema in genital or perianal area, fever, malaise
  • fournier’s gangrene
209
Q

GLP-1 example and SE

A

exenatide

GI, wt loss
usually administered SC

210
Q

glucagona like peptide-1 analogs- exmaple

A

exenatide

211
Q

montiroing needed to type 2 diabetics

A

every 3 months- HbA1c– keep below 48 mmol/L

annualy

  • foot check- sensation, ulcers, infections
  • fundoscopy
  • BP
  • cholesterol
  • kidneys- check ACR for renal dunction
212
Q

what is maturity onset diabetes for the young (MODY), tx

A

monogenic diabetes- autosomal dominant

often diagnosed in <25s, behaves like T2

tx- insulin, sulfonylurea

213
Q

causes of hypoglyaemic epidose

A

EXPLAIN

  • EXogenous drugs (insulin, alcohol, Sulphonylureas)
  • Pituitary insufficiency (low ACTH and cortisol)
  • Liver failure
  • Addison’s disease (low cortisol)
  • Iset cell tumours (insulinoma)
  • non-pancreatic neoplasms
214
Q

sx hypoglycaemic episode

A
  • syncope, dizziness
  • shaking, tremor
  • anxiety, irritability
  • hunger
  • impaired vision
  • headache
  • sweating, tachy/palpitations due to glucagon/arenaline release
  • LoC, coma, confusion
215
Q

tx hypoglycaemia

A

<4mmol/L

  • glucose liquid/tablets/ 40% gels/ fruit juice, sugar
  • avoid chocolates and biscuits
  • once >4mmol/L- give long acting CHO- biscuits, bread, milk
  • no response – IM glucagon or glucose 10% IV infusion
  • if unconsious/seizuring/aggressive- glucagon, glucose 10%/20% IV
  • omit IV/short acting insulin
  • do not omit long acting insulin
216
Q

sx DKA

A
  • N+V
  • Abdo pain
    ^ could be it!
    ____________
  • deep signing breaths- Kaussmals
  • pear drop sweat smelling breaths
  • bed wetting in prev dry chil
  • increased urinary frequency- polyuria
  • polydipsia
  • wt loss
  • pale and thin
  • drowsy, LoC
217
Q

DKA Ix

A
  • FBC UE CRP– hyponatraemia, hypokalaemia and low bicarb (acidosis) in severe cases, increased anion gap
  • ABG/UE- metabolic acidosis
  • weight pt
  • urinanaysis/serum ketones
218
Q

dka diagnostic criteria

A
  • acidaemia <7.3 or low bicarb <15
  • ketosis cap sample >3, or >2+ in urine
  • hyperglycaemia >11mol/L random
219
Q

expected ABG results during DKA

A 
pH <7.3
pO2- high >7
pCO2- low <5 
BE- low -2.5
bicarb is <15, 15-18 if mild dka
Glucose high >11
220
Q

management of DKA (adult dosages and vols)

A

Fluid

  • shock- NaCl 500ml over 15min, give another is <100mmhg systolic
  • not shocked- give 500ml-1L NaCl over an hour, then 250ml/hr until euvolaemic

Insulin

  • 50u actarapid in 50ml of NaCl (1u/ml) stat
  • continuous IV infusion 0.1u/kg/hour
  • fall in glucose should not exceed 5mm/hr

Potassium

  • start once K is normal
  • KCl 20mmol/hour
  • do no give if anuric
  • IV glucose 10% 125ml/hour when glucocse <14
  • 5000u daily of daltaparin
  • when out of DKA< switch to sliding scale insulin
221
Q

Paeds- management in DKA

A 
FLUIDS
If shocked:- bolus
- 20ml/kg over 15min
- if still shocked give 10ml/kg
- if still shocked, give inotropes

Deficit: – 48 hour volume
% dehydration x Kg x 10

Maintenance:– per day

  • 100ml/kg for first 10kg
  • 50ml/kg for next 20kg
  • 20ml/kg for remaining weight
    • up to 80kg
  • over 48 hours to reduce risk of cerebral oedema

Potassium

  • every 500ml bag contains 20mmol of K (40mmol/L)
  • monitor UEs and ECG

Insulin

  • 50u actarapid in 50ml of 0.9% NaCl (1u/ml)
  • infusion 0.05 or 0.1u/kg/hour
  • give normal long acting insulin at normal dose during DKA
  • stop usual short acting insulin whilst on infusion
  • turn off insulin pump
222
Q

what is hyperosmolar hyperglycaemic state

A
  • high serum osmolality (>320mmol/kg) due to profound hyperglycaemia (often >40mmol/L0 in the absence of an acidosis or ketosis
223
Q

presentation of hyperosmolar hyperglycaemic state

A
  • polyuria, polydipsia
  • weakness, nausea
  • wt loss
  • dehydration - dry mucous membrane, poor turgor
  • disorientation
  • drowsiness, LoC
  • tachy
  • hypotension
  • shock
224
Q

management of hyperosmolar hyperglycaemic state

A
  • fluids
  • correction of electrlytes (K)
  • IV insulin
  • dalteparin- VTE risk high
225
Q

what LT complications of diabetes are there

A
  • neuropathy (TCA/SSRIs, gabapentin, opioids, capsaicin, TENS,)
  • diabetic foot, charcot
  • motor nerve damage- clawing, callus
  • peripheral vascular disease
  • retinopathy- blurred, darkened/distortion, floaters, flashed of light, visual field loss
  • nephropathy- proteinuria, nephrotic syndrome, malaise, pruritis, oedema
226
Q

what is an adrenal crisis

A
  • occurs due to acute adrenal insufficiency (addion’s (primary), secondary (pituitary/hypothal damage))
227
Q

sx and signs of adrenal crisis

A
  • Abdo, flank pain
  • confusion
  • dizziness
  • LoC, coma
  • fatigue, weakness
  • fever
  • hypotension (low aldosterone)
  • Cardiovasc collapse
  • hypoglycaemia (low cortisol)
  • hyponatraemia (low Aldosterone)
  • hyperkalaemia ( low aldosterone)
228
Q

what is carcinoid syndrome

A
  • when neuropeptides like serotonin, histamine and postaglandins are released into circulation by neuroendocrine tumours
  • eg phaeochromocytoma, other tumours in appendix, ileum, rectum and elsewhere capable of producing these things
229
Q

sx carcinoid tumours

A
  • flushing
  • wheezing
  • diarrhoea
  • abdo pain
230
Q

management of carcinoid syndrome

A
  • octreotide (somatostatin analogue)

- tumour resection

231
Q

causes of hypertirchosis

A

hair everywhere on body

  • ciclosporin, drugs
  • congenital
  • porphyria cutanea tarda
  • anorexia nervosa
232
Q

what different serum/urine ix are used for phaeochromocytoma, conns, addisons, cushings

A

Phaeochromocytoma-

  • plasma and urinary metanephrines (breakdown product of catecholamines)
  • 24hour catecholamine urine- also an option but is less reliable than the above

Conn’s
**- aldosterone:renin serum – high (aldosterone is high, renin is low)

Adrenal insuff/Addison’s

  • 9am cortisol levels
  • *- ACTH levels (low in secondary insuff, high in Addison’s)
  • *- ACTH stimulation test (cosyntropin)- stimulates cortisol if central, both low if adrenal, both high if paraneo
  • *- Plasma renin and aldosterone levels- renin high and aldo low in Addison’s, may be normal in secondary
  • Autoantibody- 21-hydroxylase Ab, adrenal cortex Ab

Cushing’s-

  • 24hour urinary free cortisol
  • dexamethasone suppression test,
  • midnight cortisol levels
  • plasma ACTH
233
Q

which antidiabetics are assoc with wt loss and which with wt gain

A

LOSS

  • GLP-1 - SC (tide)
  • SGLT2- PO (flozin)

GAIN

  • Insulin- SC
  • Sulfonylreas- PO eg gliclazide, tolbutamide, glimepiride
  • Thiazolidinediones- PO

NEUTRAL
- DPP-4 (liptin)

234
Q

What type of cancer that causes hyperthyroidism, is inherited

A

medullary carcinoma

  • associated with MEN II
  • tx resistant HTN
  • one nodule!
235
Q

what does a hot thyroid nodule on scintigraphy suggest ? what would the TSH be?

A

toxic adenoma, could also be thyroiditis

  • low TSH due to thyrotoxicosis
  • NB- thyroid cancer rarely cause thyrotoxicosis or hot nodules!
236
Q

an 18 year old female presents with 3 nodules in the right lobe of her thyroid plus cervical lymphadenopathy. Her TFTs are normal. likely diagnosis?

A

thyroid nodules+ lymphadenopathy= papillary carcinoma

  • likely to spread to lymph nodes
  • most common type of thyroid cancer
237
Q

causes of cold nodules on thyroid sctintigraphy

A
  • cancers
  • cysts
  • fibroids
  • non functioning adenoma
  • thyroiditis
238
Q

causes of hot nodules on sctintigraphy of thyroid

A
  • toxic adenoma
  • thyroiditis
  • NOT cancer
239
Q

cause of diffuse uptake of radioisotopic iodone on sctintigraphy (diffuse hot)

A

graves

240
Q

what is MEN 1 assoc with

A

3ps

  • parathyroid (primary hyperparathyroid)
  • Pancreatic
  • Pituitary (prolactinoma, adenoma)
241
Q

what is MEN 2 assoc with

A 
2A
- medullary thyroid cancer
- phaeochrmocytoma
- Primary hyperparathyroid (hyperplasia)
2B
- medullary thyroid cancer
- phaeochrmocytoma
- Marfan or Neuromas
242
Q

what is sick euthyroid

A
  • caused by systemic illness- stem will often be person in ITU or recovering from illness in hosp
  • low thyroid hormones (mild), normal or low TSH
243
Q

what does an elevated TSH with normal T4 indicate

A

subclinical hypothyroidism

244
Q

what does a low TSH with normal thyroid hormones mean

A

subclinical hyperthryoidism

245
Q

most common cause of primary hyperaldosteronism

A

BL adrenal hyperplasia

246
Q

what type of cancer is hashimoto’s thyroidisis associated with

A

MALT lypmhoma

247
Q

most common cause of addisons in the UK, and worldwide

A
  • uk- autoimmunity (>idiopathic)

- worldwide- infection (mostly TB)

248
Q

secretion of what hormones is reduced as part of stress reposnse

A
  • insulin
  • testosterone
  • oestrogen
249
Q

what is latent autoimmune diabetes of adulthood

A

LADA

  • like T1 in older (may present with DKA
  • 30-50y
  • lack of insulin due to beta islet cell destruction
  • No family history
  • other autoimmune diseases
  • no increase in body habitus

MODY

  • like t2 but in younger
  • tend to be under 25s
  • normal insulin production, decreased sensitivity
  • less likely to present with DKA etc
250
Q

what causes hydatid cysts

A
  • tape worm (low B12 sx, pruritis, GI sx)

Dog Tapeworm:

  • Cystic echinoccosis (CE)/ hydatid disease
  • infection with the larval stage of Echinococcus granulosus
  • farming areas- raw meat fed to dogs who then spread it to us
  • on aspiration of the liver cyst, people may experience an anaphylactic like reaction, so this is not done on cysts that have a *detached membrane on CT
251
Q

what do meduallry cancer of the thyroid produce

A

calcitonin-

  • hormone made by your thyroid to control how the body uses calcium.
  • increases bone calcium content and decreases serum calcium level
  • levels are used to screen for recurrence after resection of one
252
Q

what type of diabetes does Lithium cause

A

nephrogenic diabetes insupidus

Finals (15 decks)

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