Endo SAQ Flashcards
45/M reduced libido referred to clinic, testosterone 5.7(L), LH 1.4 (Borderline L), FSH 2.6 (Borderline L), blurring of vision.
a) which cells produce testosterone in the testis?
b) Physical signs to look for (3)
c) what do the biochemical results show? (1)
d) 2 causes lead to (b) (2)
e) Ix (4)
a) leydig cells
b) gynecomastia, small testes, decreased body hair
c) causes of hypogonadism (klinfeltor syndorme, kallmann syndrome, hypopituitiarism, prolactinoma)
d) serum LH and FSH to distinguish between primary and secondary hypogonadism
Lady present with failure to express breastmilk and no return of menstruation 3 months after birth. The patient was told her failure to breastfeed is related to the septicaemia. The blood results are as follows:
FSH Normal 2.0 (1.0-10?)
LH Low? Normal? 1.2 (1.0-10?) LH is abnormally normal - borderline low normal
Estradiol: undetectable
Prolactin: low
Question 1: What are the endocrine dysfunctions in related to her complaints (2)
Question 2: What is the mechanism and what is the name of the syndrome (2)
Question 3: Found to have low ACTH and TSH, what test to diagnose the endocrine deficiency and explain the results. (4)
4. What medications to give for the ACTH and TSH deficiencies (1)
5. What medications to treat secondary amenorrhoea (1)
- failure to produce breast milk: low prolactin. Secondary amenorrhea: FSH and LH
- Postpartum blood loss + hypovolemic shock and septic shock leading to pituitary necrosis and hypopituitarism. Sheehan syndrome
- Serum ACTH and cortisol level. Short synacthen test (to test for ACTH deficiency).
- Hydrocortisone, levothyroxine
- Estrogen and progesterone (HRT)
An old woman comes in with L3 spine fracture, diagnosed to have fragility fracture and was started on alendronate.
1. Name 3 secondary endocrine causes of osteoporosis?
2. Mechanisms of alendronate, frequency given and when?
3. AE of alendronate?
4. Contraindications of alendronate?
5. Patient cannot tolerate bisphosphonate. Name 3 medical therapeis to treat post menopausal osteoporosis?
- Cushings, hyperparathyroidism, hyperthyroidism, hypogonadism, renal osteodystrophy
- Bisphosphonate inhibits osteoclast function thereby decreasing osteoclast resorption of the bone. Taken once every week and before meal to increase bioavailability (wait 30-2 hours before meal/fluids)
- GI discomfort (GI reflux, esophagitis, esophageal/gastric ulcers and gastritits)
- History of hypersensitivity to the bisphosphonate, hypocalcemia, CKD with a GFR of <30mmol/min, esophageal disorders (achalasia, esophageal strictures, esophageal varices, Barretts esopshagus), history of atypical femur fracture secondary to bisphosphonates, history of osteonecrosis of jaw secondary to bisphosphonates
- Denosumab (RANKL antibodboy), teriparatide (PTH analogue), raloxifene (SERM), romosozumab (sclerostin inhibitor)
Young man with HT, DM and HL. Currently on Enalapril, metformin, statin. Recurrent angioedema.
1. Most likely cause for his angioedema (2marks?)
2. Most appropriate management (2 marks)
3. Two questions to ask in history taking to differentiate histaminergic and bradykinin angioedema (4 marks)
4. Name an inherited condition that can cause angioedema (2 marks?)
- Enalapril associated bradykinin accumulation
- Stop ACEI and switch ACEI to ARB
- Duration of onset/offset, wheals and angioedema (histaminergic) vs angioedema only (bradykinin), response to antihistamine medication
- Hereditary angioedema/C1 esterase inhibitor deficeincy
Middle/old age woman with T2DM and anxiety neurosis. Covid vaccine 2 weeks ago. Couldn’t eat. Coffee ground vomiting once, complained of abdominal/epigastric pain. On admission, found to be dehydrated. Mild epigastric tenderness. BP117/? P7x. Working diagnosis is acute stress gastritis.
On glipizide, Metformin, pioglitazone, dapagliflozin
Previous creatinine level 50
Blood test
BG 20
Na 136, K 6
Urea 27 , Creatinine 12x
pH 7.3
O2 normal, CO2 slightly low, HCO3- 12 Low, Base excess –10
- Interpret acid-base disorder and renal function. Explain the correlation between the acid base disorder and renal function.
- Why is the urea and creatinine derangement so disproportionate
- What is the most likely cause of her renal derangement and how to manage her?
- 2 possible correlation between her DM drugs and acidosis
- 2 medications to prescribe on admission?
- Metabolic acidosis, urea creatinine is high (BUN:Cr >100). Acute kidney injury causing impaired excretion of H+
- Resorption of GI bleed, hypovolemia/prerenal failure, history of vomiting, poor oral intake
- Pre-renal failure due to hypovolemia, IV normal saline for fluid resuscitation
- Metformin: lactic acidosis, dapagliflozin: euglycemic DKA
- IV fluids for rehydration, IV normal human insulin, IV PPI
M/51, T2DM for 10yrs on 2 pre-mixed insulin and metformin. Recently added empagliflozin. Also has hypertension on 4 anti-hypertensives and hyperlipidemia on atorvastatin, Stage 3a chronic kidney disease. his BMI is 33. BP 145/90 blood tests:
Hba1c 7.8%
LDL 3.6 (pretreatment 4.2) (normal <2.6)
Liver function test normal eGFR 53 (ref range >90)
UPCR 300mg ref range <30mg/d (unit should be mg/mmol Cr?)
1. Apart from lowering glucose, list two reasons for starting empagliflozin
2. Name another diabetic agent to improve overall metabolic condition
3. Give 2 possible medical conditions to explain why hypertension is resistant to medications
4. Give two reasons why the cholesterol levels are suboptimal despite statin therapy
5. With regards to his empagliflozin, what advice will you give him if he has to undergo elective laparoscopic cholecystectomy?
- Weight loss, renal protection, cardioprotective
- GLP1 receptor agonist (exenatide, liraglutide)
- Think about secondary hypertension: OSA (obesity BMI: 33), renal artery stenosis (hyperlipidemia and atherosclerosis), chronic kidney disease, phaeochromocytoma
- Non compliance to statin therapy, familial hypercholesterolemia (statin monotherapy not sufficient)
- Stop empagliflozin 3 days before surgery, risk of euglycemic ketaocidosis (precipitated by peri operative conditions such as reduction of insulin, starvation, sepsis or dehyration)
SGLT2: glycosuria, increased ketone body reabsorption in renal tubules, decreased Na+ reabsoprtion
In addition to surgical stress which induces increased ketogenesis –> increased plasma ketone bodies –> euglycemic diabetic ketoacidosis
M/87, lower limb weak for the past 3 months(?), unsteady, did not go out due to COVID for a long time, find heavy housework tough; lower limb PE 4/5 power. The muscle bulk is decreased. He also reported an unintentional 5kg weight loss in the past 1 year.
1. 3 features for frailty phenotype in this patient?
2. 3 AE of frailty
3. 2 defining features of sarcopenia
4. 2 evidence based mx against sarcopenia
- Weakness (grip strength), slowness, low level of physical activity, weight loss (>10lb lost unintentionally in prior yera)
- Falls, disability, hospitalization, institutionalization, death
- Low muscle strength: handgrip <28kg for men; 18kg for women. Low physical performance: 6m walk. Low muscle mass: <7kg/m2 for men, <5.4 for women
- Comprehensive geriatric assessment. Excercise: resistance excercise to increased strength, mass, balance 3-5x/week. Nutritional support: protien + caloric, HMB, vit D and calcium 1000mg daily
SARM: increased tissue selectivity
Biologics under development: bimagrumab, stamulumab
a) Minor stroke+ apraxic gait in dementia, polypharmacy as diuretics (hypotension, dizziness –> orthostatic hypotension), (quetiapine (atypical antipyschotic): causes dizziness, fatigue), zopiclone (dizziness, daytime sleepiness (causing transient LOC)) is a non BDZ hypnotic/sedative
b)
MMAI (multifactorial multidisciplinary falls risk assessment and intervention program
Walking aids: umbrella
Education
Postural hypotension: fludrocortisone
Sarcopenia: protein supplement
Vit D supplement
Ca supplement
c) donepezil (acetylcholinesterase inhibitor) which improves cognition and global function with alzheimers and vascular dementia
a) hyponatremia (dilutional hypoNa from cortisol insufficiency. Note that Ald function is preserved (as aldosterone is regulated by the RAAS system) –> no hyperK)
b) panhypopituitarism (FSH/LH deficiency (hypogonadotrophic hypogonadism), ACTH deficiency
c) FSH/LH deficiency: measure serum FSH/LH
ACTH deficiency:
1 microgram short synacthen test for ACTH deficiency. dx: when decreased cortisol response to ACTH with normal or decreased basal ACTH (r/o primary adrenal insufficiency)
Insulin tolerance test (GH and ACTH deficiency): decreased GH and cortisol response to hypoglycemia. 0.1U/kg insulin –> measure glucose/cortisol at pre, 15,30,60,90,120 mins. Cortisol should elevate >500nmol/L.
d) Postural hypotension as there is hypoNa so inability to maintain BP. No cortisol so reflex increased production of CRH which an analogue of ADH –> so increased reabsorption of water –> euvolemic hypoNa.
e) FSH/LH/ACTH deficeincy caused by RT for NPC
f) Fluid restriction based on patients renal diluting capacity
a) SIADH
b) urine and serum osmolarity, urine Na, cortisol
Urine osmolarity increased, usually 2x serum osmolarity, urine Na>20mmol/L (as there is inappropriate reabsorption of water)
c)
CNS: infections (meningitis, encephalitis, brain abscess), head trauma, SAH
Respiratory: CA lung, chest infection
Neoplastic: carcinoma (bronchogenic, duodenal, pancreas, bladder, prostate), lymphma
Drugs e.g. chlopropramide (sulphonylurea), neuropsychiatric drugs (carbamazepine, SSRI, antipsychotics, amiodarone, diclofenac)
d) Remove excess water: fluid restriction/ furosemide
e) central pontine myelinolysis
a) Leydig cells
b) decreased body hair, gynecomastia, reduced testicular volume, obesity, reduced muscle mass
c) Acquired
* suppression of gonadotrophins: hyperprolactinemia, drugs, chronic systemic illness, DM
* Damage to gonadotrophic cells: benign and malignant tumor and cysts, infiltrative diseases, pituitary apoplexy, surgery/radiation to sellar region
d) FSH/LH to see if hypogonadotrophic hypogonadism (locate the level of HPA axis lesion)
A 50+ year old man presents with sudden onset bilateral lower limb weakness. Laboratory results show elevated Ca and PSA. MRI shows a lesion compressing the spinal cord. The patient is given denosumab.
a. What is the mechanism of action of denosumab?
b. What are the side effects of denosumab?
c. What immediate management will you do for the spine problem? Give 2
After the treatment you give in c, the patient’s neurology improves. Transperineal biopsy is performed and CA prostate is confirmed. The oncologist now plans to give goserelin.
d. What is the mechanism of action of Goserelin
e. What drug will you give as well when administering goserelin?
a. denosumab is a RANKL monoclonal antibody that binds to RANKL (on osteoblast) thereby preventing it from binding to RANK on osteoclast –> no osteoclastogenesis –> antiresorptive effective
b. Osteonecrosis of the jaw, atypical femoral fracture, hypocalcemia
c. Steroid (dexamethasone), surgical decompression, RT
d. LHRH analogue
e. Coadministration of a steroidal or non-steroidal antiandrogen
A 55-year-old man with impotence was found to have a serum prolactin of 25000 mU/L (normal < 500 mU/L).
(a) What is the likely diagnosis?
(b) What further investigations are required for optimal management of his problem?
(c) Name 3 treatment options.
(a) Hyperprolactinemia due to macroprolactinoma (if >5000)
(b) Visual perimetry, pituitary MRI, pituitary hormone profile
(c) Dopamine agonist (e.g. cabergoline), transphenoidal surgery if mass effect, RT if unresectable
(b) Insulin tolerance test for GH or ACTH deficiency
LH,FSH, testosterone for assessent of LH/FSH deficiency
TSH, free T4 for TSH deficiency
Short synacthen test for ACTH deficiency
A 35-year-old man was brought to the Accident & Emergency Department by an ambulance because of generalized weakness and inability to move his limbs on waking up in the morning. He was noted to have a staring look and a small goitre. His serum sodium was 140 mmol/L and potassium was
2.0 mmol/L. He had no history of severe vomiting or diarrhoea.
(a) What is the most likely diagnosis?
(b) Discuss briefly the management of this patient.
(a) thyrotoxic periodic paralysis
(b) ABC, NPO until swallowing cleared, BP/P QID.
ECG stat: any arrhythmia (changes of hypoK e.g. large U wave, loss of T wave and prolonged QT interval)
Give IV slow and diluted KCl solution
Monitor by ECG and K level (stop once normoK)
TFT early. Initiate treatmetn for Graves disease first.
PE: pulse, signs of thyrotoxicosis, neurological deficits.
Ix: TFT, RFT, and electrolytes, ABG, 24 hour urinary K and simultaneous blood and urine K for transtubular K gradient exclude renal loss.
A 36-year-old woman was found on pre=employment medical examination to have hypertension mild type 2 diabetes. She had central obesity and a rounded face with rosy cheeks. 9 am serum cortisol was 66 nmol/L (normal 130–660 nmol/L).
(a) What is the likely diagnosis?
(b) What further investigations can help you to confirm the diagnosis?
(c) What advice should you give to her?
(a) iatrogenic cushing syndrome
(b) SST to show suppressed HPA axis (1mg 3o mins short synacthen test. Expected result: low plasma cortisol after short synacthen administration due to chronic suppression of adrenal from chronic steroid use.
(c) assess if other steroids being taken. If patient is undergoing surgery recently, she should have steroid cover before to avoid adrenal crisis.
(a) adrenal insufficiency, antihyperrtensive overdose, hypoglycemia, HONK with dehydration
(b) hstix, postural BP, ECG, urine x glucose/ketone, RFT with electrolytes, serum BHBA, A/VBG, CBC xhb
(c) inadequate cortisol response (cortisol should increase) compatible with adrenal insufficency.
(d) hydrocortisone replacement in split daily dosing. Mineralocorticoid (fludrocortisone)
(e) physiological replacement still need steroid cover for OT. Must carry blue steroid card. Abrupt withdrawal = acute adrenal insufficiency
(a) What is the likely diagnosis?
(b) What physical signs would you look for?
(c) What are the abnormalities in the initial investigations and what further investigations would you perform?
(d) How would you manage this patient?
(a) adrenal insufficiency (cannot specify as Addisons: primary adrenal insufficiency)
(b) postural hypotension. Pituitary hypersecretion/hyposecretion features. hyperpigmentation if primary.
(c) hypoNa, hyperK, impaired renal function, random cortisol/ACTH, SST
(d) hydrocortisone + fludrocortisone
(a) hypercalcemia, impaired renal function (increased urea/creatinine), high ALP
(b) primary hyperparathyroidism: renal impairment from dehydration. Exogenous calcium supplement. Tertiary hyperparathyroidism. Hypercalcemia to r/o malignancy.
(c) PTH, Po4, urine ca/cr ratio to r/oFHH. DEXA, vertebral XR. S/UPEP to r/o MM
(d) if proven to be primary hyperPTH, hyperCa is an indication for OT therefore parathyroid scintigraphy (sestamibi scan) + USG for pre op localization is indicaetd
