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Its the final countdown > Endo > Flashcards

Endo Flashcards

1
Q

Goserelin is a GnRH analogue… name the gonadotophins

A

FSH and LH

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2
Q

what are 2 key findings f addisonian crisis

A

severe hypotension
electrolyte imbalances

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3
Q

what are the 3 steps in managing addisonian crisi

A
  • Aggressive fluid resus
  • IV steroids emphaisis on IV
  • Glucose (in hypoglycaemia
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4
Q

Elderly female pt w/ unilateral swelling on the neck, slowly growing larger over years
Sx: no hoarse voice/ swallowing difficlties
exam: uneven goitre, no bruit, not fixed/firm
Bloods - TFTs normal.

what is the management of the underlying cause

A

do not require tx

this is a Thyroiid cyst ( elderly female, aSx neck mss, slow growing = thyroid cyst

thyroid malignancy would have been =- fixed/firm nodule, recent enlargement, lymphadenopathy)

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5
Q

3 clinical features of diabetes insipidus

A

large volumes dilute urine (>3L dilute urine in 24hrs & urine osmolality <300mOsm/kg)

nocturia

excess thrist

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6
Q

and
—-

give 4x cuases for each

A

diabetes insipuds can be CRANIAL or NEPHROGENIC

cranial: head trauma, inflammatory conditions (sarcoidosis), cranial infection (meningitis), vascular conditions (sickle cell disease)

nephrogenic: drugs (lithium), metabolic disturubances (hypercalcaemia, hypokalaemia, hyporglycaemia), CKD.

both; rare genetic causes (Wolframs syndrome for nephrogenic diabetes insipidus )

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7
Q

stepwise management options in acromegaly

A

1st line Surgical: Transsphenoidal surgery

if surgery C/I or nto responsive to surgery: Somastostatin analogues ( octreotide, lanreoride) (1st line medical)
GH antagonist ( pegvisomant)
dopamine agonist ( bromocriptine )

aggressive & resistant to surgery/meds: radiotheray

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8
Q

50 yo female w/ uncontrolled HTN , muscle cramps and fequent urination

what electrolyte imbalance is likely to be fouund

how would this appear on an ECG

what are the 2 management options

A

electrolyte imbalance - hypokalaemia (<3.5mmol/L)

uncontrolled HTN + muscle cramps + frequent urination + hypokalaemia = hyperaldosteronism

ECG - (only where K<2.7mmom/l)
- raise Pwave
- prolonged PR interval
- widespread ST depression & Twave flattening/inversion
Prominent Uwaves( V2 and V3)
Long QT interval

uncontrolled HTN = not responding despite multiple anti-HTN

Mx:
- surgical ( if lesion/tumour)
- medical: potassium -sparin diruectics ( Amiloride, spiroolactone, eplerenone) ( in bilateral adrenal disease

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9
Q

what is the difference between hyperaldosteronism and Conns

A

Conn’s = primary hyperaldosteronism
autonomous overproduction

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10
Q

Is Hashimoto’s disease a form of hyper or hypothryoid?

What are the 3 examination findings of the thyroid in this condition>

A

hypothyroid

smooth, non-tender, goitre,

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11
Q

what is the most common cause of hyperthyoroidsi ,

how does the thyroid present

A

graves disease
Smooth goitre
( goitre = abnormal enlargement of thyrouid gland)

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12
Q

what form of thyroiditis is triggered by a viral infection?

does this cause hyper or hypothryroid

How does the thyroid present

A

De Quervain’s thyroiditis

Hypothyroid

Painful smooth goitre ( painful as it enlarges rapidly)

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13
Q

Give 3 causes of nodular goite

A

multinodular goitre, thyroid cyst, thyroid cancer

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14
Q

what examination finding suggests thyroglossal cyst?

A

rises with BOTH swallowing & tongue protrusion

(unlike e.g. hashimotos which just rises ith swallowing)

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15
Q

give clinical features of a thyroid storm

A

thyroid storm = severe thyrotoxicosis, life-threateneing form of hyperthyroid

hyroid storm
- fever, sweting, HR>140, DNV, coma

thyrotoxicosis
unexplained wieghtloss, tachycardia, arrhythmia, uscles weakness, nervsoius/anxious/irritable. shaky, heat sensitivity, menstrual changes

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16
Q

what is the immediate management in suspected post-partum thyroiditis

A

watch and wait

a) difficult to differentiate from graves
b) have 3 months hyperthyroid followed by hypothyroid ( so meds could make them unwell)

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17
Q

what group of women are at increased risk of post-partum thyroiditis

A

havign autoimmmune disease

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18
Q

Graves: What is the 2nd line Med for breastfeeding women, why can’t the 1st line be used?

A

2nd line - Betablockers
( tx thyrotoxic Sx)

carbimazole (1st line) contains propylthiouracil, which passess through breast milk

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19
Q

Graves: What is the 2nd line Med for breastfeeding women, why can’t the 1st line be used?

A

carbimazole

can cause congenital abnormalities, so Propylthiouracil used in 1st trimester, the Carbmiazole for 2nd &3rd trimester ( as propylthiouracil can cause severe hepatic injury).

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20
Q

Mx in thyroid storm

A

suportive ( IV fluids, analgesia, propanolol for tachycardia) propylthiouracil/carbimazole ( stop thyroid hormone synthesis

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21
Q

what signs are seen in hypocalcaemia

A

trousseau’s sign = carpopedal spasm caused by the inflation of a blood pressure cuff

Chvosteks sign - ipsilateral facial twitching when tappin6g on6 the contralateral cheek

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22
Q

what antibodies are found in the most common cause of hypothyroidism?

A

Most common cause of hypothyroid : Hashimotos (UK)

Ab:
anti-thyroid peroxidase (anti-TPO)
anti-thyroglobulin (anti-Tg) a

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23
Q

most common cause of hypothyroid UK, Worldwid

A

UK - hashimotos
world - iodine deficiency

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24
Q

what are the 4 tx options for hyperthyroid

A

Carbimazole ( main 1st line, but not to be used in 1st trimester)

Propylthiouracil (1st trimester, but long term causes hepatic injury)

Radioactive iodine

Thyroid surgery

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25
Q

Give 4 causes of primary hypothyroid (aside from autoimmun - Hashimotos, and iodine deficiency)

A

Lithium (inhibits T3 &T4 production)
Amiodarone
Hyperthroid Mx: Carbimazole, propylthiouracil, radioactive iodine, thyroid surgery

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26
Q

Causes of secondary hypothyoroidism ( x5)

A

Tumours: pituitary adenonma

surgery to pituitary
radiotherapy
sheehans (avascular necrosis of pituitary gland)
trauma

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27
Q

1st and 2nd line options in hypothyroid tx

A

Oral levothyroxine
- titrated every 40weeks based on TSH level

2nd Liothyronine sodium - synthetic T3 (specialist care)

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28
Q

what is subclinical hypothyroidism

A

thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low).

There may be absent or mild symptoms.

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29
Q

what is the most common cause of hypethyroid? and whag antibodies are associated with it

A

Graves - autoimmune disease

TSH receptor antibodies

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30
Q

what are the 4 causes of hyperthyroidism

A

GIST
Graves disease
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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31
Q

Give the 4 causes of thyroiditis

A

thyroiditis include:
* De Quervain’s thyroiditis
* Hashimoto’s thyroiditis
* Postpartum thyroiditis
* Drug-induced thyroiditis

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32
Q

what is the hand swelling and finger clubbing in Graves disease called

A

Thyroid acropachy

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33
Q

what are the 3 phases in De Quervains Thyroiditis

A

aka subacute thyroiditis

  1. Thyrotoxicosis
    2 Hypothyroid
    3 return to nornmal
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34
Q

what are the 4 features of the thyrotixic phase of De Quervains thyoriditis

A
  • Excessive thyroid hormones
  • Thyroid swelling and tenderness
  • Flu-like illness (fever, aches and fatigue)
  • Raised inflammatory markers (CRP and ESR)
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35
Q

what is the management in De Quervains thyroiditis

A

supportive, its a self-limiting condition

NSAIDS - sx pain/inflammation

B-blockers (hyperthyoid Sx

Levothyroixine (hypothyroid Sx)

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36
Q

what is the difference between a thyroid storm and thyrotoxici crisis

A

same thing

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37
Q

4 features of thyroid storm/thyrotoxic crisis

A

1 Features of hyperthyroidism
2 fever
3 tachycardia
4 delirium

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38
Q

Management in thryroid storm

A

same as with thyrotoxicosis ( supportive, NSAIDs for analagesia) also
- fluid resus
- anti-arrhythmic meds
- beta-blockers

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39
Q

What GI condition are patients on carbimazole at risk of ( hint: causes severe epigastric pain radiating to the back)

A

acute pancreatitis

40
Q

what acute blood condition can be caused by Carbimazole and Propylthiouracil

A

Carbimazole/ Propylthiouracil - agranulocytosis

Carbimazole - acute pancreatitis
Propylthiouracil - hepatic damage

Typical: patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

41
Q

which b-blocker is most commonly used to bloc the adrenalin-related symptoms of hyperthyroidism

A

propanolol

42
Q

what are the risks of thyrotoxicosis in pregnancy>

A

foetal loss
maternal lheart failure
premature labour

43
Q

what is the most common cause of thyrotoxicossi in pregnancy

A

Graves disease

44
Q

can radioiodine therapy be used in hyperthyroid in pregnancy?

A

no: Contraindicated

45
Q

how does the management on hypothyroidism change in pregnancy

A

thyroxine is safe in pregnancy and breastfeeding

dose should be raised

46
Q

when should pts with subclinical hypothyroidism be Tx?

A

if symptomatic, and < 65 years old.
repeat TSH & T4 conducted 3 months later, is still raised TSh w/ normal T4, give Tx

otherwise they will become hypothyroid

(subclinical hypothyroidisim: TSH is raised but Thyroid hormones are normal)

47
Q

which 5 causes of thyroid disease lead to a goitre

A

Lithium
Hashimotos
Iodine deficiency
toxic multinodular goitre/
Graves

48
Q

what is sick euthyroid syndrome

A

most commonly seen in chronically ill patients/ in starvation. TFTs are low and the patient clinically euthyroid.

49
Q

what triad of symptoms does T1DM typically present with

A

polyuria, polydipsia, weightloss ( sx of hyperglycaemia)

or DKA

50
Q

what are 3 key features of DKA

A

Ketoacidosis
dehydration
postassium imbalance (high/normal - potassium normally driven into cells by insulin, non insulin –> no cell potassium. May be normal as kidneys secrete excess)

important to correct as these are what will kill t

51
Q

what is the criteria for diagnosing DKA

A

all three of:
*Hyperglycaemia ( > 11 mmol/L)
* Ketosis ( >3 mmol/L)
* Acidosis (< pH 7.3)

52
Q

what is the management in DKA

A

FIG-PICK

Fluids - IV hartmanns, 1L in 1st hr, then 1L/2hrs

Insulin -fixed rate infusion

Glucose - closely monitor blood glucose, add infusion when <14mmol/L

Potassium - add to IV fluids and monitor closely (insulin infusion –> drives K into cells –>? hypokalaemia –> arrhythmia)

Infection - may be underlying trigger of DKA so tx

C- chart fluid balance

Ketones - monitor ketones. pH, bicarbonate

53
Q

what are the 4 key complications of DKA Mx

A
  • Hypoglycaemia
    *Hypokalaemia
    *Cerebral oedema, esp in kids
    *Pulmonary oedema (secondary to fluid overload)/ acute respiratory distress syndrome
54
Q

what autoantibodies are associated with T1DM

A
  • Anti-islet cell antibodies
  • Anti-GAD antibodies
  • Anti-insulin antibodies
55
Q

What is the longterm complication of injecting insulin into the same spot

A

lipodystrophy

56
Q

hypoglycaemia can be tx with rapid-acting glucose (high content drink), what are the medical options

A

IV dextrose and IM glucagone

57
Q

what are rhe tx targets in T2DM

A
  • 48 mmol/mol for new type 2 diabetics
  • 53 mmol/mol for patients requiring more than one antidiabetic medication
58
Q

what are the 1st, 2nd and 3rd line medical mx in T2DM

A

1st - metfromin (w/ SGLT2-i dapagliflozin if CVD as well)

2nd line - Metformin + sulfonylurea/pioglitazone/DPP-4i/ SGLT2 i

3rd line - triple therapy: metformin + 2 secondline drugs OR insulin therapy

59
Q

metformin
- 2 main SE
- does it cause hypoglycaemia
- does it cause weight gain

A

SE
GI Sx (pain, nausea, diarrhoea)
Lactic acidosis (2ndary to AKI)

Hypoglycaemia - no

weight gain - no

60
Q

SGLT-2 i

  • give 2 drug names
  • give 2 main S/E
  • what positive S/E does it have
A

suffix -gliflozin

e.g. empagliflozin, dapagliflozin

  • raised risk of thrush/UTI
  • DKA

(also hypo)

Positive: improves HF and CVD

61
Q

which diabetic meds cause a risk of hypo

A

SGLT-i (eg dapaglitazone)
sulfonyluria (gliclazide)
insulin

62
Q

According to the (DVLA) guidelines, are insulin-treated diabetics allowed to drive heavy goods vehicles (HGVs)

A

yes, if they fulfil very STRICT criteria

  • there has not been any severe hypoglycaemic event in the previous 12 months
  • the driver has full hypoglycaemic awareness
  • the driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving
  • the driver must demonstrate an understanding of the risks of hypoglycaemia
  • here are no other debarring complications of diabetes
63
Q

what is the 1st line Mx for HTN any T2DFM patient

A

ACEi (also used in CKD)

64
Q

how does HHS ( hyperosmolar hyperglycaemic state) present?

A

hyperosmolality (from water loss, so blood very concentrated),

hyperglycaemia

absence of ketones (so not DKA)

present with: polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension, confusion

65
Q

what 2 measurements are used to screen for diabetic nephropath

A

albumin: creatinine ratio
U&Es

66
Q

what is the management in diabetic nephropathy

A

ACEi - for HTN and diabetic nephropathy

optimising Blood glucose

67
Q

what is the difference between hyperaldosteronism and Conns syndrome

A

hypersaldosteronism high levels of aldosterone

conns - high levels of adolsterone due to adrenal adenoma

68
Q

what is the key presenting feature of hyperaldosteronism

A

hypertension

69
Q

what is the role of aldosterone

A
  • Increase sodium reabsorption from the distal tubule
  • Increase potassium secretion from the distal tubule
  • Increase hydrogen secretion from the collecting ducts

(so overall hypokalaemia)

70
Q

what are the 3 causes of primary hyperaldosteronism

A

bilateral adrenal hyperplasia ( most common)

adrenal adenoma (Conn’s syndrome)

Familial hyperaldosteronism (rare)

71
Q

what will
aldosterone
renin

levels look like in
primary hyperaldosteronism
secondary hyperaldosteronism

A

primary
aldosterone: high
renin: low ( suppressed by raised BP)

secondary
aldosterone: high
renin: high renin stimulates the release of aldosterone

measured by “plasma aldosterone/renin ratio”

72
Q

give 3 causes of secondary hyperaldosteronism

A

secondary - raised renin

  • Renal artery stenosis
  • Heart failure
  • Liver cirrhosis and ascites
73
Q

give 4 investigations used in hyperaldosteronism

A

aldosterone-to-renin ratio
screeining for primary aldosteronism ( renin low, aldosterone high)
vs secondary (renin high, so aldosterone high)

BP (hypertension)
Hypokalaemia (as aldosterone excretes K for Na retention)

ABG/VBG - alkalosis ( as aldosterone secretes H+)

74
Q

what are the appropriate Ix for hyperaldosteronism (x3)

A

CT/MRI - adrenal tumour/hyperplasia

Renal artery imaging (doppler US/CTA/MR angiography) - renal artery stenosis

Adrenal vein blood sampling (both adrenal glands)

1st line ix - aldosteron-rening ratio, THEN CT abdo & adrenal artery sampling to differentiate between uni and bilateral disease

75
Q

what is the management in hyperaldosteronism (x3)

A

Aldosterone antagonists (eplerenone/spironolactone)

tx underlying cause (surgery in adenomal, percutaneous renal artery angioplasty in stensosis )

76
Q

what is the most common endocrine cause of secondary hypertension

A

hyperaldosteronism ( inc. conns)

expect in younger people/ failure to respond to tx / hypokalaemia

77
Q

what form of neurological disturbance is found in diabetic peripheral neuropath

A

sensory ( not motor) *may also cause pain

in glove and stocking distribution (legs affected first) “ having loss of sensation on both of his legs up to his knees and some sensory loss in his fingertips.

78
Q

there are 4 drug options in diabetic neuropathy

A

neuropathic anbalgesics:
amitriptyline, duloxetine, gabapentine, pregabalin

tramadol as rescue med in exacerbations

79
Q

aside from sensory loss, what other neuropathic complication occurs in diabetes

A

gastrointestinal autonomic nueorpathy - gastrioparsis (Sx: erratic blood glucose control, bloating, vomiting)

80
Q

what is the Mx of diabetic- related gastroparesis

A

prokinetic agents - metoclopramide, domperidone or erythromicin

81
Q

what HBA1C indicates prediabetes
- %
- mmol/mol

A

42-47mmol/mol

5.7 - 6.4 %

82
Q

what HbA1c indicates diabetes
- mmol/mol
- %

A
  • > 48mmol/mol
  • > 6.5%
83
Q

what is the recommended HBA1c treatment target in new TIIDM pts

A

48mmol

84
Q

what is the recommended treatment target for diabetic pts on 2 or more antidiabetic medication

A

53 mmol/mol

85
Q

cause of cushings

A

prolonged high levels of glucocorticoids ( cortisol)

86
Q

what is the difference between cushing’s disease and cushing’s syndrome

A

cushings disease - pituitary adenoma secretes excess ACTH

cushing syndrome - prololonged cortisol from any source including exogenous sortisol ( prednisolone or dexamethasone)

87
Q

give 5 metabolic conditions that may arise in people with cushings

A

HTN
Cardiac hypeertrophy
TIIDM
Dyslipaedaemia
osteoporosis

88
Q

causes of cushings syndrome

A

CAPE

Cushing’s disease -pit adenoma, high ACTH
Adrenal adenoma
Paraneoplastic syndrom
Exogenous steroids

89
Q

high levels of which hormone ( in Cushings / primary adrenal insufficiency) causes skin pigmentation

A

ACTH - allows you to determine the cause as excess ACTH, either from Cushing’s disease or ectopic ACTH

90
Q

what test is used to diagnose cushings syndrome

A

dexamethasone suppression test

normal: dex given –> negative feedback (hypothalamus; CRH)–> negative feedback ( pit. ACTH) –> cortisol suppression

91
Q

there are 3 dexamethasone tests used to test for cushings syndrom; which is used to screen for to exclude cushings syndrome

A

low dose overnight test

1mg dex given 10/11pm
checked at 9am
normal - supressed cortisol
abnormal - not supressed –> further assessment required

92
Q

there are 3 dexamethasone tests used to test for cushings syndrom; which is used to test for cushings syndrome

A

low-dose 48-hour test
dex (0.5mg) taken every 6hrs ( 8 doses)
cortisoll levels checked
- 9am day 1
- 9am day 3

normal: cortisol production supressed

93
Q

there are 3 dexamethasone tests used to test for cushing’s syndrome; which is used to determine the cause of cushing’s syndrome

A

high -dose 48 hour test
dex (2mg) taken every 6hrs ( 8 doses)
cortisoll levels checked
- 9am day 1
- 9am day 3

Cushings disease ( pit. adenoma) - cortisol supressed
adrenal adenoma/ ectopic ACTH - not supressed

94
Q

Tx in cushings syndrome

  • cushings disease
  • adrenal tumour
  • ectopic tumour
A

cushings disease - transphenoidal pituitary adenoma removal

adrenal tumour - surgical removal

ectopic tumour producing ACTH - surgical removal

otherwise, bilateral adrenalectomy and life-long steroid replacement therapy

95
Q
A

Its the final countdown (23 decks)

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