Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MBChB - Full Clinical Topics > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Jacky, 30, has had a range of persisting symptoms, which doctors believe is down to hypoadrenalism. Which symptom would distinguish between primary adrenal failure and secondary adrenal insufficiency?

A

Skin hyperpigmentation

Seen in primary adrenal insufficiency (as this will have high ACTH)

Not seen in secondary as this has low ACTH

Hyperpigmentation is caused by melanin stimulating hormone (which has same pre-cursor as ACTH)

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

Name 4 common features of multiple myeloma

A 
CRAB
C- hyperCalcaemia 
R- Renal failure 
A - Anaemia (and thrombocytopenia)
B - Bone fractures or lytic lesions or bone pain

Investigate: Serum elecrophoresis looking for a monoclonal band

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

What presenting symptoms and investigation results characterise diabetes insipidus?

A

Polyuria and polydipsia
High serum osmolality and low urine osmolality

(High urine osmolality would rule out DI)

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

What steroids are highly mineralocorticoid and which highly glucocorticoid? What side effects do each have?

A

Mineralocorticoid = Fluid retention, HTN
- Fludrocortisone

Glucocorticoid = Immune suppresion plus all normal steroid SE (endocrine, GI, pysch, cushings etc)
- Dexamethosone

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

What is indicated by raised ferritin levels?

A

Either iron overload (10%)
OR
Inflammation (90%) - note ferritin is an acute phase protein

Transferin saturation <50% excludes iron overload

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

A 41-year-old woman presents with palpitations and heat intolerance. On examination her pulse is 90/min and a small, diffuse goitre is noted which is tender to touch. Thyroid function tests show the following:

Free T4 24 pmol/l
TSH < 0.05 mu/l

What is the most likely diagnosis?

A

Thyrotoxicosis with tender goitre = subacute (De Quervain’s) thyroiditis

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

Name 3 ECG changes associated with hyperkalaemia?

A

Prolonged PR
Wide QRS
Peaked/ tented T waves

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

What are the three categories and six most common causes of hyponatremia?

A

Na < 135

Hypovolemic: Diuretics or Addisons
Euvolemic: SIADH
Hypervolemic: Heart/ liver/ renal failure

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

How do you treat hyponatremia in acute and chronic situations?

A 
PLUS TREAT UNDERLYING CAUSE
Acute (<48hrs) = 3% hypertonic saline 
Chronic:
- Hypovolemic = 0.9% isotonic saline 
- Euvolemic = Fluid restriction
- Hypervolemic = Fluid restriction (plus furosemide if underlying condition warrants it)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the symptoms of hyponatremia? (5)

A 
Confusion, headache, balance difficulty
Altered mental status
Seizures/ coma 
Orthostatic hypotension 
Low urine output, decreased JVP, dry mucus membranes, poor skin turgor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the most common causes of hypernatremia? (5)

A

Water loss
- Hyperglycemia
- Loop diuretics
- Diabetes insipidus (not enough ADH to reabsorb water)
- Severe diarrhoea, sweating, burns, vomitting etc
Not enough water gain
- Limited intake of water
Sodium gain
- Cushings (= increased glucose, sodium retention with the water retention)
- Primary aldosteronism (resets regulation of ADH secretion)

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

How do you manage hypernatremia?

A

Oral or IV fluids

Plus treat underlying cause

  • If water loss may need desmopression (Diabetes insipidus)
  • If excess sodium and fluid overload may need loop diuretic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the definitions of hyperkalaemia?

A

Mild - 5.5-5.9 mmol/L.
Moderate - 6.0-6.4 mmol/L.
Severe - >6.5 mmol/L.

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

What are the main causes of hyperkalaemia? (4 groups)

A

DRISP
Drugs (ACEI, ARBs, NSAIDS, heparin)
Renal (AKI/ CKD/ addisons)
Increase in production (Tumour lysis syndrome, trauma, burns)
Shift from intracellular to extracellular (DKA)
Pseudo (long tourniquet time, clenched fist, test tube haemolysis)

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

Name 3 symptoms of hyperkalaemia?

A

Usually non specific weakness and fatigue

Can get muscle paralysis, SOB and bradycardia

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

What investigations should be done on a patient with hyperkalaemia? (4)

A 
Repeat K+
ECG
Glucose 
FBC
ABG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name 3 changes on an ECG associated with hyperkalaemia?

A 
Peaked T waves
Prolonger PR (>200)
Wide QRS (>120)

Hyperkalaemia can cause conduction disturbances!

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

How should hyperkalaemia be managed is K+ is 7.1?

A

SEVERE: Urgent ABCDE
- ABG to give immediate determination if true result, perform ECG

1) 10ml 10% Calcium gluconate to protect heart (works in 1-3mins, lasts 30-60mins). Keep giving upto 50ml until ECG improvement

2a) Insulin-glucose infusion (10units with 25g glucose) - moves K+ into cells. NB: K+ should come down 0.5-1 over 15mins
2b) Nebulised salbutamol (10-20mg should reduce K+ 0.5-1mmol/L in 15-30mins)

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

How should a K+ of 5.9 be treated?

A

Use calcium resonium (gets K+ out of GI tract, brings down by approx 1mmol but takes 2 hours so no use in acute setting)

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

How is hypokalaemia classified?

A

Mild - 3.1-3.5 mmol/L
Moderate - 2.5-3.0 mmol/L
Severe - <2.5 mmol/L

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

What are the three most common causes of hypokalaemia?

A 
Increased water loss:
- Diuretics
- Vomiting/ diarrhoea 
Cellular shift:
- Alkalosis
- Insulin/ glucose
Decreased K+ intake:
- NBM
- Anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does hypokalaemia present?

A

Generally asymptomatic

Can give weakness, muscle pain, constipation or paralysis

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

What are the findings in an ECG for a patient with a K+ of 2.9?

A

ECG changes in hypokalaemia:

  • Flat T waves
  • ST depression
  • Prominant U waves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is hypokalaemia managed? (2)

A

If mild: Dietary suppliments (40-120mmol/day)

If secondary care and severe:
- IV KCL (never bolus, give with normal saline). Needs careful monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
You are called to the ward to see a patient with high sugars, roughly how much does 1 unit of insulin cause a BM to drop?
1 unit drops blood glucose by approx 3mmol Remember aiming around 8-10
26
Name 3 rapid acting insulins? When are they used?
Humalog Novorapid Apidra Fiasp All act rapidly (within 20mins) and have short action (<6hours) Good for meal time insulin and correcting insulin
27
When should biphasic insulins be given?
At meal times | As contain rapid and intermediate acting insulins
28
What is the definition of hypoglycaemia?
Under 3mmol however in practice any under 4 should be treated
29
What is a phaeochromocytoma and how does it present?
Neuroendocrine tumor of the medulla of the adrenal glands Present: Raised BP, palpitations, sweating, anxiety
30
What investigation is done for phaeocrhomocytoma?
24 hr urinary metanephrines
31
What is the treatment pathway for phaeochromocytoma?
A- Alpha blocker B- Beta blocker C- Cut it out (surgery)
32
How does congenital adrenal hyperplasia present and what is the most common cause?
Kid with precocious puberty and possible sex changes Due to 21-hydroxylase deficiency
33
What investigation should be done for congenital adrenal hyperplasia?
17-hydroxyprogesterone
34
What is the function of vasopressin?
Vasopressin = ADH Causes retention of water (solute free)
35
What is diabetes insipidus and how can causes be categorised?
Diabetes insipidus = not enough ADH (so no stopping of diuresis = lots of diuresis) Therefore presents with polyuria and polydipsia Cranial cause - Not producing ADH in post pituitary Renal cause - Not responding to ADH
36
What is seen on plasma and urine osmolarity in diabetes insipidus?
Plasma osmolality = High | Urine osmolality = Low (as lots of fluid in urine so it's dilute)
37
What is the first/ second line investigation of diabetes insipidus?
1) Water deprivation test Would expect urine osmolality to rise, if it DOESN'T then this is DI (if it does probably pyschogenic cause of polydipsia) 2) Desmopressin test - Giving ADH should put things back to normal (raised urine osmolarity). If it does then this is pituitary cause of the DI, if it doesn't the kidneys aren't responding to any ADH so renal cause
38
How do you manage diabetes insipidus?
Cranial cause = Give desmopression (ADH) | Renal cause = Supportive, protect kidneys, desmopression may help a bit
39
What is the action of aldosterone?
Promotes water reabsorbtion (via Na+ absorbtion and K+ excretion) - So spironolactone which inhibits aldosterone causes less reabsorbtion (lowerBP) and less K+ excretion (which is why can cause hyperkalaemia)
40
What are the features of acromegaly (increased growth hormone 2ndry to pituitary adenoma)
Spade hands, increase show size Large tongue Excessive sweating and oily skin Pituitary tumour > Headaches, bitemporal hamianopia
41
How do you investigate a patient for suspected acromegaly?
GH varies throughout day so not diagnostic Do OGTT with serial GH measurements - Normal = GH supressed <2 with hyperglycaemia - Acromegaly = No supression of GH
42
How is acromegaly managed?
Trans-sphenoidal surgery Can use somatostatin (GH inhibiting hormone) analogues (octreotide) as an adjunct before surgery
43
What are the diagnostic criteria for T2DM?
HbA1c > 48mmol/l Fasting glucose > 7mmol/L OGTT > 11.1mmol/L 1 result if symptomatic, 2 if asymptomatic
44
What are the result options for a fasting glucose?
``` <6.1 = Normal 6.1-7 = Impaired fasting glucose >7 = Diabetes ```
45
What are the result options for an OGTT?
``` <7.8 = Normal 7.8-11.1 = Impaired glucose tolerance >11.1 = Diabetes ```
46
What are the driving rules with diabetes?
Ok to drive but if more than 1 episode of hypo which required assistance need to contact DVLA
47
What are the characteristics of a DKA presentation?
Abdopain, polyuria, polydipsia, pear drop breath, kussmaul breathing, N+V, reduced GCS Acidosis <7.3 Ketones in urine Glucose >11mmol (Diagnositic criteria)
48
How should DKA be treated?
ABCDE Fluids (1L in 1hr, 1L in 2hrs, in 4hrs, in 8hrs) Insulin (0.1/units/kg/hr) - Once glucose under 15mmol/l start 5% dextrose also Investigations for cause: FBC, blood cultures, CXR CT head if reduced GCS Note needs continually reassessing
49
What is the presentation of HHS?
General weakness, leg cramps, confusion, hypovolemia Criteria: Glucose >30mmol/l Hyperosmotic >320mOs/l Hypovolemia Often no acidosis!
50
How is HHS treated?
Slow fluid rehydration - Watch for reducing osmolarity - Only use insulin if acidosis
51
Name 5 presenting symptoms of diabetes?
``` Polyuria Polydipsia Lethargy Pruritus Frequent infections ```
52
What are your first four steps in T2DM management?
1) Lifestyle 2) If HbA1c still over 48mmol/l = Start metformin 3) If HbA1c still over 58mmol/l = Start 2nd - Sulfonylurea (Gliclazide, glipizide, glimepiride) - DPP-4/Gliptins (Sitagliptin) - Thiozolidianoes (Pioglitazone) - SGLT-2 inhibitor (Dapagliflozin) 4) Add third drug from above
53
What is 5th line management in T2DM?
If HbA1c still >58mmol/L on 3 drugs - If BMI <35 = Start exanitide (GLP-1 analouges) OR - Start insulin
54
What are pre and post prandial targets for T1DM?
``` Pre-prandial = 4-7mmol/l Post-prandial = <9mmol/l ```
55
What are the characteristics of MODY?
``` Young age T2DM Autosomal dominant (HNF-1alpha) ```
56
What is the best 1st line tx for MODY?
Sulfonylureas (Gliclazide) NOT metformin
57
What is the action of glucagon?
Increases glucose to increase blood sugar
58
What are the characteristics of SIADH?
``` No peeing (So high urine osmolarity) Diluted plasma (So low serum osmolarity) Often have hyponatermia ```
59
How is SIADH treated?
Depending on cause (Hypo/eu/hypervolemic)
60
What is addisons disease?
Primary adrenal insufficiency (low cortisol and low aldosterone)
61
What are the features of addisons disease?
Lethargy, weakness, N+V, weight loss, salt craving Hyperpigmentation (raised ACTH) Hypotension, hyperkalaemia, acidosis, hyponatremia (all due to low aldosterone) Hypoglycemia (due to low cortisol)
62
How do you investigate possible adissons disease?
Short syncanthen test (give ACTH) - Normal = Cortisol will rise >550 within 30mins - Addisons = Adrenals not working so no rise in cortisol
63
How is addisons disease treated?
``` Replace glucocorticoid (hydrocortisone) Replace mineralocorticoid (fludrocortisone) ```
64
Other than addisons name three other causes of hypoadrenalism?
Primary (Mets, TB, HIV) Secondary (Pituitary tumour, radiation) EXOGENOUS GLUCOCORTICOID THERAPY
65
What is Conn's syndrome?
Primary hyperaldosteronism CAUSED by an adrenal adenoma | i.e. all Conn's is PH but not all PH is Conn's
66
What are the three key features of primary hyperaldosteronism?
Hypertension Hypokalaemia Alkalosis
67
What is the first line investigation for primary hyperaldosteronism?
Aldosterone/ renin ratio | will be raised in primary hyperaldosteronism
68
How do you manage primary hyperaldosteronism?
If Conn's = Surgery (take out adenoma) If due to bilateral adrenocortical hyperplasia (70%) = Spironolactone
69
What are the components of the HPA axis?
Hypothalmus >(CRH)> Pituitary >(ACTH) > Adrenals > (Cortisol)
70
What are the 4 most common causes of cushings syndrome?
Exogenous = Iatrogenic (steroid therapy) ``` Endogenous: Cushing disease (80%) - Pituitary tumour releasing ACTH Adrenal adenoma (10%) Ectopic ACTH (5%) i.e. from SCLC ```
71
Name 5 features of cushing syndrome?
``` Weight gain Moon face Truncal obesity Easy brusiing Hirsuitism Proximal muscle weakness Facial plethora ```
72
What 2 investigations can be performed to diagnose cushing syndrome?
Urinary 24hr free cortisol (>280nmol/24hrs = CS) ``` Low dose (1mg) dext supression test Normal = Cortisol reduces CS = No reduction ```
73
How do you distinguish between pituitary or adrenal causes of cushing disease?
High dose (8mg) dex supression test Pituitary cause = Decrease in ACTH and decrease in cortisol Adrenal cause = Decrease in ACTH but NO decrease in cortisol
74
What are the most common causes of an addisonian crisis? (3)
Sepsis Surgery Steroid withdrawal
75
How should an addisonian crisis be managed?
1) 1L saline over 1hr (with dextrose if hypoglycemic) 2) IV hydrocortisone
76
What are the components of a diabetic foot exam?
``` Look (Skin, ulcers, swelling) Feel (Temp, cap refil, pulses) Move (+gait) + Sensation ```
77
Name 3 features of a hyperthyroid crisis (thyroid storm)?
Hyperpyrexia (>41) Tachycardia (>140) N+V, jaundice, diarrhoea, abdo pain, confusion, agitation
78
How should you treat a hyperthyroid crisis (thyroid storm)?
1) ABCDE (oxygen, fluids etc) 2) IV propanolol 5mg 3) Carbimazole or propylthiouracil PO 4) Hydrocortisone If agitation - chlorpromazine
79
What is myxoedema coma?
Extreme manifestation of (usually untreated) hypothyroidism ``` > Hypothyroid features + Apathy, low mood, confusion, cognitive decline and possible coma Hypothermia (<35.5) Hypotension, bradycardia ```
80
How should myxoedema coma be managed?
ABCDE - Early HDU/ ICU admission - Immediate T4 and T3 given IV - IV hydrocortisone - Broad spectrum AB's Correct electrolyte and fluid abnormalities
81
Name 7 common hyperthyroid symptoms?
``` Weight loss Heat intolerance Tachycardia Diarrhoea Oligomenorrhoea Sweats Tremor Irritability and agitation ```
82
Name 7 common symptoms of hypothyroid?
``` Weight gain Cold intolerance Bradycardia Constipation Menorrhagia Myalgia/ cramps Weakness Thin hair Dry skin Low mood ```
83
What are the 4 most common causes of hyperthyroidism?
Graves (70%) Toxic multinodular goitre Subacute (DeQuevains) thyroiditis - post viral Toxic adenoma
84
What are three common features of graves disease?
Age 40-60 Exopthalmos, opthalmoplegia, lid lag, pretibial myxoedema (TSH receptor antibodies in 90%)
85
How do you manage hyperthyroidism?
Propanolol for rapid symptom relief Then either: A - Slowly titrate carbimazole (or propriothiouracil if preg) according to TFT's B- High dose carbimazole to block and levothyroxine to replace Tx for 12-18months then slowly withdrawl 2nd line - Radioiodine 3rd line - Thyroidectomy
86
What are the 6 most common causes of hypothyroidism?
Primary atrophic thyroid Hashimoto's (Goitre + TPO antibodies) Iodine deficiency (Worldwide most common) Drugs/ surgery (amiodarone/ lithium) Sick euthyroid (precipitated by illness) - Low TSH Pituitary tumour - Low TSH
87
What is sub-clinical thyroid disease and how is it managed?
Low or high TSH with a normal T3/T4 - Treat if symptomatic, otherwise observe 6 monthly
88
How do you treat hypothyroidism?
Levothyroxine (0-100mcg) | - Half life is 7 days so wait 4 weeks between changing doses
89
What is the most useful marker to monitor progression of a thyroid carcinoma?
Serum thyroglobulin
90
What are the most common types of thyroid cancer?
``` Papillary carcinoma (70%) - Young females, excellent prognosis Follicular adenoma (20%) ```
91
How should papillary carcinomas or follicular adenomas of the thyroid be managed?
Total thyroidectomy Followed by radioiodine Yearly thyroglobulin levels to detect early recurrent disease
92
What is the typical bone profile and clinical features of primary hyperparathyroidism?
Bone profile: - Raised PTH, raised Ca, low Phosphate Clinical: Asymptomatic or recurrent abdo pain (pancreatitis/ renal colic)
93
What is the most common cause of primary hyperparathyroidism?
Adenoma (80%)
94
What is the typical bone profile and clinical features of secondary hyperparathyroidism?
Bone profile: - Raised PTH, low Ca, high phosphate, low VitD Clinical features: - Bone disease (Secondary hyperparathyroid often due to CKD)
95
What is the most common cause of secondary hyperparathyroidism?
CKD
96
How is primary hyperparathyroidism managed?
Surgery
97
How is secondary hyperparathyroidism managed?
Medical | Calcium and vitD supplimentation
98
How do you differentiate between primary atrophic hypothyroid and hashimoto's?
Primary - No goitre | Hashimoto's- Goitre, likely TPO antibodies
99
What is the second line diabetic management drug (after metformin) most commonly for a) Obese patients and b) non-obese patients?
a) Sitagliptin (DPP-4 inhibitor) - weight neutral b) Gliclazide (sulfonylurea) - normally best but can cause weight gain (so not in obese) also causes hypo's so not those at high risk
100
Which acid causes acidosis in DKA?
β-hydroxybutyric acid
101
In the cori cycle, where is glucose converted to lactate and vice versa?
Glucose > lactate = In liver | Lactate > Glucose = In skeletal muscle

MBChB - Full Clinical Topics (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions