Endocrine Key Flashcards
1
Q
Thyrotoxicosis (Hyperthyroidism) in pregnancy
A
:
* Propylthiouracil is preferred preconception (before pregnancy if a woman
is planning to get pregnant) and in the first trimester and postpartum.
Carbimazole
is preferred in 2nd and 3rd trimesters + in general (non-
* Carbimazole pregnant).
- Carbimazole: risk of aplasia cutis and omphalocele in the fetus.
- Propylthiouracil: risk for hepatotoxicity in the mother
- Both drugs can cross the placenta; so, use the lowest possible dose.
2
Q
Hyperthyroidism in pregnancy
A
- Radioiodine therapy is contraindicated during pregnancy.
- If hyperthyroidism cannot be controlled by drugs
→ Partial thyroidectomy can be done in the 2nd trimester.
However, the safest Rx modality for pregnant women with hyperthyroidism
is by giving antithyroid medications (e.g., PTU).
3
Q
2ry adrenal insufficiency (mostly iatrogenic).
A
• After a long period of steroids intake,
a sudden cessation of steroid intake
will lead to 2ry adrenal insufficiency (iatrogenic).
• Look for unexplained abdominal pain + nausea, vomiting
± postural hypotension ‘’
Dizziness, Falls’’
.
Note that (1ry adrenal insufficiency = Addison’s disease, will be discussed in
the coming keys).
4
Q
Diabetic ketoacidosis:
- Occurs mostly in DM type 1
A
Abdominal pain,
vomiting,
Kussmaul breathing (deep hyperventilation),
dehydration,
glucose>11.
- Management:
√ Initially → Iv fluids
√ followed by “ Iv infusion of insulin plus measure ABG
Sometimes, ABG is not given,
VBG is given -venous blood gases-
”
N.B. Sometimes, these options are not given,
pick (measure capillary blood glucose) Obviously!
- Dx: (pH < 7.3),
ketonemia > 3 or ketonuria ++,
Glucose > 11,
Bicarb < 15
The initial fluid therapy in a patient with diabetic ketoacidosis is:
→ 500 ml of 0.9% sodium chloride over 15 minutes. “bolus”. (0.5 L, not 1 L).
5
Q
Osteomalacia
A
Low ca
Low phosphate
High ALP
6
Q
Hyperkalemia
Tall Tented T wave,
Prolonged QRS → Hyperkalemia
Once these ECG changes occur → give IV calcium gluconate or calcium chloride
A
- Tall Tented T wave, Prolonged QRS →
- Firstly, protect the cardiac membrane by giving
IV Calcium Gluconate or Calcium Chloride).
- Then, reduce the serum Potassium
by giving sometimes Insulin with dextrose
Or sometimes Salbutamol inhalation.
7
Q
A
8
Q
Acromegaly:
A
◙ In acromegaly, there is excess growth hormone (GH)
secondary to a
pituitary adenoma in over 95% of cases.
◙ Some important features:
- Bitemporal hemianopia, “due to compression on optic chiasm”.
- spade like hands,
- enlarged nose and jaw.
- large tongue,
- prognathism “an extension or bulging out (protrusion) of the lower jaw
(mandible)” - interdental spaces
- Headaches,
Hypertension,
Sweating.
9
Q
Acromegaly initial testing and definitive testing
A
◙ Initial (screening) test and F/U test
(insulin like growth factors).
→ IGF-1
The most definitive (confirmatory test)
→ OGTT with serial Growth Hormone measurements.
OGTT = Oral Glucose Tolerance Test
N.B
In normal people, Growth hormone is suppressed by Glucose.
10
Q
Acromegaly features in qns
A
In acromegaly, Growth hormone is not suppressed by Glucose.
Note,
bitemporal hemianopia (due to compression of the pituitary tumor
on the optic chiasma)
is seen in several conditions, importantly:
√ Acromegaly.
√ Hyperprolactinemia (e.g., pituitary macroadenoma).
Headaches
+ Hypertension
+ Sweating
+ ↑ Insulin-like growth factor (IGF-1)
Think → Acromegaly.
11
Q
A
12
Q
Hypercalcemia with Prostate cancer.
A
- Hypercalcemia manifestations:
Polyuria,
polydipsia (↑ thirst),
confusion,
depression
and “low mood”
, kidney
stones,
abdominal pain,
constipation,
bone pain
(Moans, Groans, Stones, Bones).
- In a prostate cancer patient with these
manifestations,
initially order → serum calcium.
- The main causes of hypercalcemia:
1ry hyperparathyroidism,
Malignancy,
Sarcoidosis,
TB
- Initial management of hypercalcemia
→ Rehydration with IV fluid 0.9% normal saline (0.9% NaCl).
- Then: Bisphosphonates (
e.g. Alendronate,
Risedronate,
Pamidronate).
13
Q
Amenorrhea with HYPOTHYROIDISM:
A
- Hypothyroidism Features:
Weight gain in spite of decreased appetite,
intolerance to cold
, lethargy,
puffy face, hands and feet (myxoedema),
bradycardia,
dry coarse cold skin,
constipation, hair loss.
N.B.
initially, there is menorrhagia (↑ menstrual bleeding) followed by
oligomenorrhea or amenorrhea.
The note to remember from this key is that Amenorrhea can be associated
with Hypothyroidism.
• The Commonest cause of Hypothyroidism in the UK
→ Autoimmune hypothyroidism (Hashimoto thyroiditis).
Sometimes,
Hashimoto thyroiditis is given in the options instead of
hypothyroidism. Pick it if the features are suggestive.
• The Commonest cause worldwide: iodine deficiency (nutritional cause)
(In both causes, there is usually goitre)
14
Q
Hyperprolactinemia
A
(Milk discharge in non-pregnant woman + Amenorrhea)
The main cause → Pituitary Adenoma → do MRI brain.
MRI may also show Pituitary Adenoma
pressing the optic chiasma, leading
to a visual defect,
which is → Bitemporal Hemianopia.
- Remember: in
pituitary adenoma and acromegaly, the visual defect is
→ Bitemporal hemianopia.
- Remember: Hyperprolactinemia
→ Amenorrhea (low FSH and LH),
Galactorrhea (Milk-discharge from nipple).
15
Q
Diabetic patient suddenly collapsed and fell unconscious
A
→ Request Random Blood Glucose.
Hypoglycaemia, clinically significant when blood glucose levels fall below 4
mmol/L, can impair cognitive function,
particularly when levels drop below
3.0 mmol/L. In any patient presenting with altered consciousness,
confusion, or coma,
hypoglycaemia should always be considered.
Important Features of Hypoglycemia
→ (
Tachycardia,
Sweating,
Confusion,
Trembling,
Altered Mentation)
If blood sugar is below 4 mmol/L → It is hypoglycemia
16
Q
A
17
Q
Management of Hypoglycemia (Important)
A
Can swallow = can tolerate orally, not vomiting.
• If Conscious and Can swallow (can tolerate orally)
→ give 200 ml fruit juice Or Oral glucose gel
• If Unconscious → IV Glucose OR (In case of IV access is already put).
Conscious but Cannot swallow
OR IM or SC glucagon 1 mg (2 tubes) (
In case of IV line is not available or not
put yet or difficult to put as in patients who are having seizure/ convulsions).
18
Q
Hypoglycaemia
A
◙ In-Hospital Management of Hypoglycemia (Summary):
• If the patient is confused but able to swallow → glucose gel (can be
squeezed into the mouth between the teeth and gums).
• If the patient is confused and unable to swallow → IM glucagon or
if there is
already an IV line then give IV glucose.
Sometimes, a question will not tell you if the patient is able to swallow or not.
However, you may find in the stem that the patient has been vomiting. Thus,
he cannot swallow (cannot tolerate orally
19
Q
Hypoglycaemia RX
A
).
Examples of Used Concentrations (Important):
IV Glucose
Over 10 minutes
75 ml of 20% glucose
150 ml of 10% glucose
Over 15 minutes
100 ml of 20% glucose
200 ml of 10% glucose
Every 1-2 minutes
50 ml of 10% solution given every 1-2 minutes until patient
is conscious
or 250 ml has been given (5 times repetitions).
20
Q
Glucagon in hypoglycaemia
A
√ Glucagon is ineffective with alcohol-related hypoglycemia.
So, if the cause of
hypoglycemia is alcohol
→ insert IV access and administer IV glucose.
√ Oral glucose gel should never be used in unconscious patients because of the
fear of chocking.
21
Q
Causes of hypoglycaemia
A
◙ Some Causes of Hypoglycemia:
• Alcohol
• Liver failure (impaired gluconeogenesis).
• Excess paracetamol or aspirin.
• Sulphonylureas (e.g., glibenclamide, gliclazide).
22
Q
In sort:
• Small cell cancer of the lung → SIADH & Cushing.
• SCC of the lung → Hypercalcemia.
Adenocarcinoma of lung vs scc
A
SCC (squamous cell carcinoma) of the lung leads to → Hypercalcemia.
- This occurs (due to paraneoplastic effect as SCC releases parathyroid like
molecules (PTH) like molecules → hypercalcemia
Important:
• SCC of bronchus (lung) → PTH like molecules → Hypercalcemia.
.
Important:
• Small cell lung cancer
→ SIADH → ‘’dilutional’’ hyponatremia
→ High ADH (AntiDiuretic Hormone)
and Hypokalemia.
• It can also cause High ACTH → (Cushing).
23
Q
DM type 2 in an obese patient with impaired renal function.
A
→ Give insulin (or) (DDP4 inhibitors)
Gliptins
Why the other options are contraindicated in this patient?
• Sulphonylureas (e.g., Gliclazide): is also contraindicated → Give (gliptin or) (DDP4 inhibitors)
• Biguanides (metformin): although it reduces weight and
it is
considered the first line hypoglycemic drug for DM type 2,
it is
contraindicated in renal impairment (GFR< 30) and
the dose should be
reduced if GFR<45.
• Sulphonylureas (e.g., Gliclazide): is also contraindicated.
in renal
impairment as it increases the risk of hypoglycemia
it increases weight and the patient is already obese.
√ With bad kidneys, avoid MS (Metformin, Sulfonylurea)
• Glitazones (Pioglitazone):
it increases weight.
• SGLT-2 inhibitors:
Contraindicated if GFR<60
24
Q
A
25
2ry amenorrhea (cessation of menstruation for > 6 months after it has been
established)
that occurs with stress,
excessive exercise or
significantly low
BMI
2ry amenorrhea (cessation of menstruation for > 6 months
after it has been
established) that occurs with
stress,
excessive exercise or
significantly low BMI
If a lady presents with amenorrhea (after it has been established) +
Hx of
stress/ excessive exercise (e.g., a runner, a sports lady)
Think → hypothalamic amenorrhea imp”
26
Hypothalamic amenorrhea
Findings
- Hypothalamic failure can occur in
(stress,
excessive exercise,
low BMI).
- In Hypothalamic Amenorrhea
→ HIGH PROLACTIN.
- In hypothalamic failure →
↓ GnRH (Gonadotropin releasing hormone) →
↓ FSH, ↓ LH (with often subsequent ↓ estrogen).
27
Pheochromocytoma:
- A rare adrenal tumour secreting catecholamines (epinephrine and
norepinephrine).
- The key word is (EPISODIC).
- Features:
HTN (Hypertension),
headache,
sweating,
tremors,
palpitations,
anxiety.
Mnemonic
PHEochromocytoma:
• P → Palpitations
• H → Headache, Hypertension
• Ph → Flushing (sweating)
• E → Episodic (Paroxysmal).
28
Rx pheochromocytoma
Catecholamines,
ie, epinephrine (adrenaline) and norepinephrine
(noradrenaline).
* Dx →
24 hours collection of urine metanephrines (not catecholamines).
If 24-hour metanephrines are not in the options,
pick 24 hours
catecholamine.
* To confirm → MRI (look for adrenal tumour).
* Rx of choice
→ Surgical resection of the adrenal tumour.
* N.B. 7-10 days before the surgery, stabilize the Hypertension by giving
Alpha-blockers (Phenoxybenzamine)
followed by Beta-blockers
(Propranolol) to prevent intra-operative hypertensive crisis.
29
A case of:
DM type 2 + Microalbuminuria +
mild HTN
+ Hypercholesterolemia
What to give?
Metformin (to control Blood glucose) +
• ACEi (to reduce the BP and to slow the progression of the kidney
damage ‘’evidenced by the microalbuminuria and DM type 2’’
+
• Statin (for hypercholesterolemia).
Important: DM type 2 + HTN → always consider impairment exists.
ACEi unless severe renal
ACE inhibitors are reno-protective,
and with DM, there is a risk for
nephropathy.
Thus, we give ACE inhibitors to slow the progression of
nephropathy.
30
A 54 YO man known case of DM and HTN on metformin, ramipril and
bisoprolol. His blood pressure is 135/88 and his BMI is 30 kg/m2.
His
labs:
Urea 7 (Normal: 2-7) ▐
Creatinine 140 (Normal: 70-150)
eGFR 65 (Normal >90)
▐ HbA1c 52 (Target: < 48)
Remember these Important points:
♦ If the patient has new Dx of DM 2, advice firstly for lifestyle modifications.
If after this, his HbA1c is still > 48 → start 1 hypoglycemic (e.g., metformin).
♦ If the patient is already on Metformin, and his HbA1c is still high but < 58
Also → Advice for lifestyle modifications.
31
Adding OHA
If the patient is already on Metformin, and his HbA1c is ≥ 58
→ Add another hypoglycemic agent.
The patient in this stem belongs to the second point.
He is already on
metformin but still a bit hyperglycemic.
As his HbA1c is <58,
the answer would be
→ continue the same management +
encourage lifestyle and diet changes.
(Recently asked Q)
32
Lifestyle advice in DM
◙ So, when to advise for lifestyle modifications?
√ Newly diagnosed patient with DM 2. +
√ Already on metformin and his HbA1c < 58 (not very high).
◙ When to consider adding another hypoglycemic agent?
√ If he is on a hypoglycemic agent e.g. metformin but his HbA1c is ≥ 58.
33
A case of:
Uncontrolled DM 2 despite lifestyle changes
+ eGFR <30
+ Hx of Heart Failure
+ BMI ≥ 30 (obese)
◙ What to give?
→ Insulin
◙ Why the other options are not correct?
√ Biguanides (metformin) → contraindicated if eGFR < 30.
√ Sulphonylureas → contraindicated in obese + in impaired eGFR
√ Gliptins (DDP 4 inhibitors) → contraindicated in Heart Failure.
√ Pioglitazone (Glitazones) → contraindicated in obese, HF, Bladder cancer.
34
35
Gliptins can be given in renal impairment but not in heart failure
36
Ci and oha
√ Biguanides (metformin) → contraindicated if eGFR < 30.
√ Sulphonylureas → contraindicated in obese + in impaired eGFR
√ Gliptins (DDP 4 inhibitors) → contraindicated in Heart Failure.
√ Pioglitazone (Glitazones) → contraindicated in obese, HF, Bladder cancer.
37
OHA mnemonic
Important Mnemonics for Hypoglycemic Agents*
• With bad kidneys (GFR < 30), do not use MS (Metformin, Sulphonylureas
e.g. gliclazide, glibenclamide).
• The heart has 4 chambers, so with Heart Failure (and pancreatitis), do
not use DDP4 inhibitors (gliptins).
• The Pie (Pioglitazone) comes with the die (Risk of bladder cancer). So,
Pioglitazone has a risk for Bladder Cancer.
Pioglitazone is also
contraindicated in Heart Failure.
• Hypoglycemics that cause weight gain (↑) are SPR:
(Sulphonylureas, Pioglitazone, Repaglinide).
The rest cause weight loss (↓) except DDP4 inhibitor Which has no effect
on the weight.
• SPR without the P have risk of hypoglycemia: Sulphonylureas and
Repaglinide.
38
39
1ry Adrenal insufficiency (Addison’s disease
Mnemonic:
Hypotension, Hyponatremia, Hypoglycemia.
The only hyper is K+ (Hyperkalemia) and Hyperpigmentation.
± There is: Metabolic Acidosis
):
• Low Cortisol and Aldosterone.
• Features: A patient with:
√ Postural hypotension (dizziness and vertigo),
√ Weakness and fatigue,
√ Nausea, vomiting, abd pain,
√ Hyperpigmentation of the skin and the mucous membranes.
• The commonest cause in the developed world → Autoimmune.
• The commonest cause in the developing world → TB (infection).
40
◙ In Addison’s disease (1ry adrenal insufficiency):
- High ACTH → Hyperpigmentation
- Low Aldosterone → Hyponatremia and Hyperkalemia
- Low Cortisol→ postural hypotension and Hypoglycemia.
Please, note that in secondary adrenal insufficiency (occurs mainly after
sudden cessation of prolonged steroid intake),
there is NO
hyperpigmentation of skin and mucous membrane.
◙ Investigations of Addison’s disease
In a patient with suspected Addison’s disease, the definite investigation
Short ACTH stimulation test (
short Synacthen test).
is an →
Plasma cortisol is measured before and 30 minutes after giving Synacthen
250ug IM.
Adrenal autoantibodies such as anti-21-hydroxylase may also be
demonstrated.
If an ACTH stimulation test is not readily available (e.g. in primary care),
then sending a 9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely.
< 100 nmol/l is definitely abnormal.
100-500 nmol/l should prompt an ACTH stimulation test to be performed
Associated electrolyte abnormalities are seen in around one-third of
undiagnosed patients:
hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis
41
◙ Investigations of Addison’s disease
In a patient with suspected Addison’s disease, the definite investigation
Short ACTH stimulation test (short Synacthen test).
is an → Plasma cortisol is measured before and 30 minutes after giving Synacthen
250ug IM.
Adrenal autoantibodies such as anti-21-hydroxylase may also be
demonstrated.
If an ACTH stimulation test is not readily available (e.g. in primary care),
then sending a 9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely.
< 100 nmol/l is definitely abnormal.
100-500 nmol/l should prompt an ACTH stimulation test to be performed
42
Associated electrolyte abnormalities are seen in around one-third of
undiagnosed patients:
hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis
43
◙ Management of Addison’s disease
Patients who have Addison’s disease are usually given
glucocorticoid and mineralocorticoid replacement therapy.
This usually means that patients take a combination of:
√ Hydrocortisone: usually given in 2 or 3 divided doses. Patients typically
require 20-30 mg per day, with the majority given in the morning dose.
√ Fludrocortisone.
Patient education is important:
√ Emphasise the importance of not missing glucocorticoid doses.
√ Consider MedicAlert bracelets and steroid cards.
Management of intercurrent illness
In simple terms, the glucocorticoid dose should be doubled.
44
Addison’s disease vs adrenal crisis( addisonian crisis)
Addisonian crisis = Adrenal Crisis
• Addisonian crisis, or adrenal crisis, is a potentially life-threatening
condition that results from an acute insufficiency of adrenal hormones
(glucocorticoid or mineralocorticoid) and requires immediate treatment.
• It is important to differentiate an Addisonian crisis from Addison Disease
which has a more gradual course.
• An illness or acute stress can precipitate adrenal crisis in the setting of
Addison’s disease.
• Addison’s Disease is a condition in which the adrenal glands do not
produce enough steroid hormones and occurs over several months.
What is Acute adrenal failure (Addisonian crisis)?
Sometimes the signs and symptoms of Addison’s disease may appear
suddenly. Acute adrenal failure (Addisonian crisis) can lead to life-
threatening shock.
45
Signs and symptoms of Addisonian Crises:
√ Severe weakness “excessive tiredness”
√ Confusion.
√ Pain in lower back or legs.
√ Severe abdominal pain, vomiting and diarrhea, leading to dehydration.
√ Reduced consciousness or delirium.
√ Hypotension.
√ High potassium (hyperkalemia) and low sodium (hyponatremia).
√ Hypoglycemia can also be seen.
i.e. shortage (↓) of 3S → Salt (low Na+ but high K+), Sugar, Steroids.
46
Causes of adrenal crisis
• Sepsis or surgery causing an acute exacerbation of chronic insufficiency
(Addison’s, Hypopituitarism).
• Adrenal haemorrhage e.g. Waterhouse-Friderichsen syndrome (fulminant
meningococcaemia).
• Steroid withdrawal.
47
Management of Addisonian crises:
First step
Management of Addisonian crises:
First step → IV Hydrocortisone 100 mg (intravenously). Important √
It can be given IM if no IV access is possible.
Hydrocortisone would correct
hypotension,
hyponatremia
and hyperkalemia.
Then → 1 litre normal saline
infused over 30-60 mins or with dextrose if hypoglycaemia
Continue hydrocortisone 6 hourly until the patient is stable.
No
fludrocortisone is required because high cortisol exerts weak
mineralocorticoid action.
Correct hypoglycemia if present.
Oral replacement may begin after 24 hours and be reduced to
maintenance over 3-4 days.
48
49
Congenital Hypothyroidism
• Important Complication → Jaundice
√ Congenital hypothyroidism is rarely seen nowadays as there are screening
tests when a baby is 6-8 weeks old (a part of the newborn blood spot test).
√ If not corrected early, it may lead to some complications such as:
• Prolonged Physiological Jaundice (starts after 24 hrs of birth and lasts for
long time)
• FFT (failure to thrive),
• Short stature,
• Impaired mental development
• Broad Flat nose,
widely set eyes,
protruding tongue.
50
51
DM type 1 with DKA
presented unwell with altered level of consciousness
and tachycardia
with signs of dehydration (Dry MM, hypotension, slow
capillary refill)
.
First investigation → Capillary blood glucose then
Arterial Blood Gas.
52
Alcohol with HYPOGLYCEMIA.
Alcohol is the commonest cause of hypoglycemia in adults followed by
treated diabetes.
- Scenario Example:
A young adult was found outside a local pub with semiconscious
level
, profuse sweating,
diaphoretic skin,
GCS 12/15,
tachycardia
and hypotension.
Hypoglycaemia
The likely diagnosis is → (He might have drunk so much alcohol → hypoglycemia).
- Dx of Hypoglycemia: Whipple’s Triad
53
- Dx of Hypoglycemia: Whipple’s Triad
1) Low plasma glucose (usually < 4).
2) Manifestations of hypoglycemia: e.g.,
sweating, confusion,
tachycardia, hypotension, altered mentation.
3) If blood glucose is corrected → rapid resolution of symptoms occurs.
54
Important Mnemonics for Hypoglycemics*
Important Mnemonics for Hypoglycemics*
• With bad kidneys (GFR < 30), do not use MS (Metformin,
Sulphonylureas).
• The heart has 4 chambers, so with HF (and pancreatitis), do not use
DDP4 inhibitors (gliptins).
• Also, the Pie (Pioglitazone) comes with the die (Risk of bladder cancer).
So, Pioglitazone has a risk for Bladder Cancer.
Pioglitazone is also contraindicated in HF.
• Hypoglycemics that cause weight gain (↑) are SPR (Sulphonylureas,
Pioglitazone, Repaglinide).
The rest cause weight loss (↓) except DDP4
inhibitor Which has no effect on the weight.
• SPR without the P have risk of hypoglycemia: Sulphonylureas and
Repaglinide.
• SGLT-2 inhibitors (Gliflozin) have increased risk for euglycemic DKA.
• SGLT-2 inhibitors (Gliflozin) have an important side effect to
remember
→ Genital infections eg, balanoposthitis (erythema and
itchiness on the penis glans and prepuce).
55
→ Think 1ry hyperaldosteronism = (Conn’s syndrome). (Adrenal Adenoma)
Think of Conn’s if:
- hypertension + Hypokalemia (e.g. muscle weakness) OR:
- Refractory hypertension despite 3 or more antihypertensive drugs OR:
- Hypertension before the age of 40 years.
- Other possible manifestations:
Weakness, Lethargy
, Headache
◙ bilateral idiopathic adrenal hyperplasia
is the cause in up to 70% of
cases.
56
57
◙ Investigations of 1ry hyperaldosteronism (Conn’s)
• Plasma aldosterone/renin ratio is the first-line investigation in suspected
primary hyperaldosteronism.
• The aldosterone: renin ratio should be checked in primary
hyperaldosteronism and should show high aldosterone levels alongside low
renin levels (negative feedback due to sodium retention from aldosterone).
• Following this a
high-resolution CT abdomen and adrenal vein sampling
is
used to differentiate between unilateral and bilateral sources of
aldosterone excess
If asked about the most suitable hormone to order
in a patient with
Hypertension and Hypokalemia ± Headaches, weakness, lethargy
→ Aldosterone.
Another valid answer → Aldosterone : renin ratio.
58
Finding in conns syndrome and Treatment
Rx: give aldosterone antagonist (e.g. Spironolactone) before considering
surgery (Adrenalectomy
Conn’s → excess (↑) Aldosterone →
Hypertension,
Hypokalemia (might be
normokalemia),
Normal Na+ or upper normal,
Headache, Weakness
± METABOLIC ALKALOSIS
± Polyuria (due to aldosterone escape)
59
Addisons
Conns
Pheochromocytoma
Remember:
√ In Addison’s (↓ cortisol and aldosterone)
→ Hyperkalemia,
Hypotension and
Metabolic Acidosis.
√ In Conn’s (↑ Aldosterone)
→ Hypokalemia,
Hypertension
and Metabolic Alkalosis.
√ In PHEochromocytoma
(↑ catecholamines: adrenaline, noradrenaline)
→ The first three letters
(PHE + F)
Palpitations, Headache, Hypertension
,
Flushing (sweating), Episodic “attacks”.
60
OHA in surgery minor and major
(◙) Pre-op Management of •
If major surgery: Stop oral hypoglycemic the night before surgery.
• If minor surgery: Continue the same routine.
Alternative: if minor procedure (e.g., upper GI endoscopy) and the patient
is on oral hypoglycemic e.g., gliclazide
→ Omit the morning dose, restart once the patient is eating and drinking
again.
61
62
(◙) Pre-op Management of DM 1 (insulin-dependent):
• If major surgery: Start sliding scale IV insulin before surgery and continue
until diet per-mouth is re-established.
• If minor surgery: Omit insulin on the day of the surgery.
In all cases, restart the previous regimen when per mouth diet is re-
established +
Check Blood glucose 4 hourly.
63
Diagnosing Diabetes
• One abnormal value,
+ DM Symptoms (polyuria, polydipsia, Unexplained wt loss in DM 1)
OR:
• Two Abnormal values without symptoms.
◙ What are the abnormal values?
◙ What are the abnormal values?
Fasting blood glucose (FBG) ≥ 7 mmol/L (≥ 126 mg/dL).
OR
Hb1Ac ≥ 48 mmol/mol (≥ 6.5%).
• Pre-diabetes (Impaired Glucose Tolerance):
Fasting → 5.5-6.9
▐ 2-hour Post-Prandial → 7.8-11
▐ HbA1c → 42-47
• Note: OGTT (Oral Glucose Tolerance Test) is the diagnostic test for
gestational DM (in pregnancy)
64
NOTE): Diagnosis of DM:
If a patient presents with polyuria, polydipsia, +ve glucose in urine
→ measure FASTING Blood Glucose, NOT RANDOM.
Note, FBG is cheaper and is usually used
while HbA1C is more expensive
and so it is usually used if there is uncertainty.
However, both are right
options for diagnosing DM but the former is to an extent is more preferre
65
Alcohol can cause hypoglycemia
(confusion,
unable to speak,
impaired GCS
or even coma)
Next Step → Check Blood glucose. √
Remember, the causes of hypoglycemia (Glucose < 4):
* Drugs: sulphonylureas, excess paracetamol, aspirin.
* Alcohol intoxication, Liver failure (impaired gluconeogenesis).
* Addison’s disease (hypoglycemia due to low cortisol).
66
MODY (Maturity Onset Diabetes in the Young)
DM Y/O
• Strong FHx (2 generations)
• Mild Hyperglycemia
• No need for insulin initially. Responds to Sulphonylureas.
→ Refer to endocrinology for
→ Genetic counselling for maturity onset diabetes in the young (MODY).
This is usually done before performing genetic tests.
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Addison’s electrolytes:
Low Na+, High K+
• Remember: in Addison’s disease (1ry adrenal insufficiency), all are hypo
except potassium:
Hyponatremia,
hypoglycemia,
hypotension (Dizziness) +
HYPERKALEMIA
+ N, V, Abd pain.
Another hyper is tanned skin
(Hyperpigmentation) but it is only seen in 1ry
not 2ry adrenal insufficiency.
• (Low Cortisol, Low Aldosterone).
- High ACTH → Hyperpigmentation
- Low cortisol → hypoglycemia and arterial hypotension
- Low Aldosterone → Hyponatremia and Hyperkalemia
- High K+ → High H+ → Metabolic Acidosis
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Cushing’s disease is not the same as Cushing’s syndrome.
Remember, in Cushing’s disease:
ACTH is supressed by low (Overnight) or
high dose of dexamethasone
In Cushing disease (e.g., pituitary adenoma), excess ACTH is released from
the pituitary gland and
travels to BOTH adrenal glands making them secrete
large amounts of cortisol.
So, Bilateral (NOT UNILATERAL) adrenal hyperplasia might occur.
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◙ Mnemonic for Cushing Syndrome Features:
“CUSHING”
• C – Central obesity,
Cervical fat pads, Collagen fibre weakness “proximal
muscle weakness”,
Comedones (acne), Cataract “due to hyperglycemia”.
• U - ↑↑ Urinary free cortisol and glucose.
• S – Striae (Broad violaceous striae), Suppressed immunity (↑ infection
liability).
• H – Hypercortisolism,
Hypertension,
Hyperglycemia,
Hypercholesterolemia,
Hirsutism
Hypertension usually that requires >2 antihypertensive agents.
• I – Iatrogenic (Increased administration of corticosteroids: a cause)
• N – Non-iatrogenic (Neoplasms: a cause)
•G – Glucose intolerance, Growth retardation
Others: • Hypernatremia (↑Na+) •
Hypokalemia (↓K+) •
Easy bruising
• Moon face and buffalo hump “due to ↑fat”
• Cardiac hypertrophy •
Osteoporosis •
Weakness and fatigability
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Cushing syndrome Investigations.
- The outpatient initial screening test → 24 hours urinary free cortisol.
The best initial test to establish the Dx
→ 1 mg (low-dose) =
Overnight Dexamethasone Suppression test.
- To localise the lesion (to differentiate between pituitary adenoma and
ectopic source →
High dose dexamethasone suppression test.
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High acth - ectopic, pituitary adenoma,scc lung, carcinoid tumour
Low acth, high cortisol- (not related to pituitary )
Adrenal adenoma mostly or excess intake of cortisol
◙ Explanation for Clarification
• Note that ACTH is released from pituitary gland while glucocorticoids
(cortisol) is released from adrenal glands.
• Therefore, if ACTH is high, there is either pituitary adenoma (Cushing
disease)
or ectopic source that secretes ACTH such as small cell lung cancer.
After performing high-dose dexamethasone suppression test, if the cortisol
is suppressed, this means that the pituitary has stopped secreting ACTH (i.e.
the problem is pituitary adenoma).
Contrarily, if it is not suppressed, then
there is another source of ACTH such as small cell lung cancer or carcinoid
tumours.
• On the other hand, if there is high cortisol, yet the ACTH level is low,
then
there is nothing to do with the pituitary gland.
The problem is either
adrenal adenoma (which secretes excess cortisol)
or maybe the cortisol is
being received from outside (excessive intake of cortisol).
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ACTH high and low
Investigations required for diagnosing pituitary adrenal adenoma or ectopic acth producing tumours
√ ACTH is released from pituitary and from ectopic ACTH releasing tumor
such as small cell lung cancer.
√ Cortisol (glucocorticoids) is released from adrenal glands.
◙ If ACTH is low, this rules out pituitary and ectopic causes →
the high
cortisol is either due to adrenal tumor (go for adrenal CT),
or excess cortisol
intake.
◙ If ACTH is high,
go for high dose dexamethasone suppression test to know
whether it is pituitary adenoma or ectopic tumor (e.g. small cell lung ca):
√ If suppressed (low cortisol),
this is Cushing disease → go for pituitary MRI.
√ If not suppressed (still high cortisol), this is ectopic
→ CT chest, abdomen.
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Vomiting
Electrolyte changes
Vomiting → Metabolic Alkalosis (due to loss of H+
-gastric hydrochloric acid-)
→ the body will keep CO2 which is acid to compensate the loss of H+ (by
hypoventilation)
→ High pH (Alkalosis),
High PCO2 (Compensatory Hypoventilation)
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Hyperkalemia can occur
2ry to Acute Kidney Injury (low eGFR) with ECG
changes: Tall Tented T-wave and Widened QRS
Initial step? → Protect the cardiac membrane before doing anything else by
or + Cardiac monitoring (as
giving there are ECG changes).
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‘Dm diagnosis
DM Diagnosis.
The first thing to do in a patient with deep painless heel ulcer, polydipsia,
polyuria, Wt loss, fatigue → request Blood sugar
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Stress hyperglycaemia
Stress Hyperglycemia:
occurs in some diseases (
e.g. Pneumonia,
MI,
Stroke)
or post-op and resolves simultaneously soon.
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Severe post-op hyperkalemia
(An important reason to remember is due to acute kidney injury 2ry to HF).
Say that the K+ is >6.4 → we need to push it intracellularly quickly as this
may lead to life-threatening arrhythmia
→ give insulin + glucose
Give 10 units insulin in 50 ml of 50% glucose IV infusion over 30 minutes
(N.B. if calcium gluconate is in the options, give it first to protect the heart)!
√ Remember: crackles at lungs, sacral edema → think of Heart Failure (Do
not give IV fluid)!
He is already overloaded due to the HF!
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Hyperkalemia RX
√ Remember: will move K+ inside the cells
temporarily (for 2-6 hours).
Therefore, IV NS (Normal Saline) needs to be
given (if not an overloaded patient e.g. HF!)
√ If the patient is well hydrated (fluid overload like in HF),
start or increase
the dose of loop diuretics (Furosemide) OR give Calcium Resonium.
N.B. In Acute Renal failure + Anuria + severe Hyperkalemia
(Especially if ≥ 7.5) → Consider Hemodialysis.
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Hypercalcemia in breast ca
Breast cancer → bone metastasis → increased thirst)
N.B. hypercalcemia (Drowsiness and
Fluoxetine like all other SSRI (used for depression) can cause
→ Hyponatremia,
however. excessive thirst presents with hypercalcemia not due to , hyponatremia. (be careful)!
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Addisons disease
Remember,
in Addison’s (high ACTH, low cortisol, low aldosterone):
HypOnatremia,
HypOglycemia,
HypOtension,
HypeRkalemia
+ Metabolic
acidosis,
N, V, Abd pain. +
Hyperpigmented skin.
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Cushing disease
Cushing’s disease is not the same as Cushing’s syndrome.
In Cushing disease (e.g., pituitary adenoma), excess ACTH is released from
the pituitary gland and
travels to BOTH adrenal glands making them secrete
large amounts of cortisol.
So, Bilateral (NOT UNILATERAL) adrenal hyperplasia might occur.
Remember, in Cushing’s disease: ACTH is supressed by low (Overnight) or
high dose of dexamethasone.
◙ Cushing features:
Hypertension that requires > 2 antihypertensive agents,
Truncal obesity,
Hyperglycemia,
moon face,
striae,
cardiac hypertrophy,
osteoporosis,
liability to infections…etc
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Toxic nodular goitre
√ Note, if the TSH is normal →
non-toxic goitre (usually no symptoms).
√ If local compressive symptoms (eg, voice changes, difficult swallowing)
→ Subtotal thyroidectomy.
Toxic nodular goitre.
• A lump on the front of the neck that moves on swallowing +
manifestations of hyperthyroidism
Think → Toxic nodular goitre.
• Some S&S of hyperthyroidism:
Palpitations,
tachycardia
, intolerance to heat,
weight loss
(unintentional weight loss despite having good appetite),
restlessness,
nervousness,
sweating.
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Panic attacks + Palpitations + Hypertension + Tremors
→ Think of pheochromocytoma
• PHEochromocytoma:
Palpitations, Headaches,
Hypertension, Flushing,
EPISODIC + Tremors and Anxiety.
• It is a rare catecholamines secreting tumours (adrenal).
• 10% bilateral 10% malignant 10% extra-adrenal 10% familial 10%
without HTN.
• Ix: 24-hour urine collection of metanephrines.
• Surgical removal of the adrenal tumor is required,
but 1-week pre-op,
stabilize the Hypertension by (e.g. phenoxybenzamine)
followed by beta-blockers (propranolol)
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Subacute thyroiditis (De Quervain’s Thyroiditis):
- Tender and painful thyroid that may radiate to the lower jaw
- (Remember: itis = painful),
- No enlargement,
- Thyroid auto-antibodies → Negative (it is inflammation, not
autoimmune disease).
- Radioactive iodine uptake test → decreased (depressed) radionuclide
uptake.
(Note, in Graves’ disease, radioactive iodine uptake is increased
whereas in subacute thyroiditis it is decreased)
• As there is Negative thyroid Antibodies
→ it is neither (Grave’s) nor
(hashimoto).
These 2 conditions are autoimmune (ie, have auto-Abs).
Subacute thyroiditis usually follows URTI (Viral).
However, in some stems,
this info won’t be given.
Instead, the stem would mention that the thyroid
is PAINFUL and radioactive iodine uptake test is DECREASED.
The picture of subacute thyroiditis:
Initially:
Hyperthyroidism (High T3 and T4, and low TSH,
perspiration-
sweating-,
palpitations, tremors) followed by
hypothyroidism.
• Remember:
in Graves (Hyper) and Hashimoto (Hypo) → +ve thyroid
antibodies.
• Rx: self-limited
As it is painful and inflammatory, NSAIDs can be used
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Subacute thyroiditis and RX of hyperthyroid state
Also, Beta-Blockers (e.g., Propranolol) can be used to control arrhythmia
and palpitations “imp”.
• Note: the patient won’t benefit from Carbimazole or propylthiouracil
as subacute thyroiditis is a transient condition.
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Thyroid crisis
Thyroid storm (Thyroid crisis)
• Precipitated by infection (e.g., chest pneumonia):
• Sick patient with low GCS, palpitations, tremors, tachycardia, feeling
warm → (thyrotoxicosis).
• Coughing, High temperature → (chest infection).
• Atrial Fibrillation may be seen on ECG may occur 2ry to thyrotoxicosis.
◙ What to give to manage palpitations?
(e.g., Oral or IV).
→ Beta-Blockers Propranolol ◙ The useful anti-thyroid medication in thyroid storm → Propylthiouracil.
(Remember that if there is no thyroid storm and no pregnancy, Carbimazole
is the first-line medication for thyrotoxicosis)
◙ N.B. Commence broad-spectrum IV Antibiotics as well for the infection
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Eye signs of Grave’s disease, what to do?
Eye signs
Lid lag
Lid retraction
Exophthalmos
Opthalmoplegia
Pretibial myxedema
Thyroid acropatchy
→ TFT
(Thyroid Function Tests are superior to Autoantibodies as we need to
establish the diagnosis of hyperthyroidism before looking for its aetiology).
◙ Important Autoantibodies in Grave’s Disease:
• Anti-thyroid stimulation hormone receptor antibodies (Anti-TSHR-Ab) are
most specific for Grave’s disease.
• Anti-thyroid peroxidase antibodies (Anti-TPO-Ab) can be found in Grave’s
but not specific for it.
They are most commonly found in Hashimoto’s
thyroiditis (autoimmune hypothyroidism).
90
◙ Important Notes on Diagnosing Grave’s Disease:
• The initial test for Grave’s Disease is → Thyroid function test.
• The most specific diagnostic test for Grave’s disease is
→ Anti-thyrotropin
receptor (Anti-TSH receptor) antibodies. On the other hand,
anti-TPO
antibodies are associated with various autoimmune diseases, not only
Grave’s.
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Hypoglycaemia
Hypoglycemic episode in a diabetic patient who presents with:
Drowsiness,
Confusion, Fatigue
, Tremors,
Blurred vision
and Sweating.
Immediately check (Random Blood Glucose).
N.B. NOT Fasting blood glucose! NO TIME!
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(Tingling, numbness, paraesthesia, involuntary spasms of upper
extremities) after Thyroidectomy → Hypoparathyroidism →
Hypocalcemia
√ When parathormone ↓ → serum calcium also ↓.
√ (after surgical removal of thyroid, parathyroid gland/s may be removed or
injured →
↓ Parathyroid hormone → ↓ Calcium
Hypocalcemia causes:
Osteomalacia (Vit D Deficiency)
Chronic Renal Failure,
Hypoparathyroidism (esp. post-op “Post Thyroidectomy”),
Hypomagnesemia,
Hyperphosphatemia.
↓ PTH → ↓ Calcium → ↑ Phosphate
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• Features of Hypocalcemia:
SPASMODIC **Neuronal Hyperexcitability**
Spasms,
Perioral Paraesthesia,
Anxious,
Seizures,
Muscle tones increased
in smooth muscles,
Orientation impaired and confusion,
Dermatitis,
Impetigo Herpetiform (rare and serious),
Chvostek’s sign,
Cardiomyopathy (prolonged QT interval on ECG).
- Trousseau’s signs → after occlusion of brachial artery → wrist flexion
- Chvostek’s sign → Tapping over parotid → twitching of facial muscles.
• Rx: give 10 ml of 10% Calcium Gluconate (initially).
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SIADH: Syndrome of Inappropriate Antidiuretic Hormone
Hyponatremia √ Can occur 2ry to small cell lung cancer → Water retention
→ Dilutional → The patient is overloaded (overhydrated)
√ Can also occur 2ry to meningitis.
√ The mainstay Rx → Fluid Restriction.
√ If failed → Tolvaptan or Demeclocycline.
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Subacute thyroiditis
• Palpitations, tremors and sweating (features of hyperthyroidism) usually
after URTi
• Imp: it can also occur in a woman after birth (Postpartum Thyroiditis
).
Postpartum thyroiditis:
An inflammatory condition of the thyroid gland, can occur after childbirth.
It includes 2 phases: starts with hyperthyroidism (the treatment is
supportive by giving propranolol
: for palpitation, tremor, anxiety),
and
second phase is hypothyroidism (levothyroxine can be given if symptomatic
hypothyroidism).
Then, it returns to normal.
• Thyroid is usually tender but not significantly enlarged.
• T3 and T4 high or upper normal (hyperthyroid phase).
• TSH low or lower normal,
• Radionuclide uptake is depressed.
➔ Give Beta-blockers (propranolol) to control palpitations and tachycardia.
N.B., we give Beta-blockers in thyroid storm and subacute thyroiditis (for
racing heart).
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Severe hyperkalemia
In all patients with severe hyperkalemia (K+ more than 6.5),
the INITIAL step
is to protect the heart by giving IV calcium gluconate or IV calcium chloride.
• Do not get tricked by haemodialysis in the options. You need to protect
the heart First!
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Impaired glucose tolerance
Impaired glucose tolerance (PRE-DIABETES):
• FBG:5.5 – 6.9 (below 7) AND:
• 2-hour Postprandial: 7.8 – 11
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Severe dehydration
A baby with severe dehydration (
dry mucous membranes,
sunken eyes and
fontanelles,
reduced skin turgor
) + HypOnatremia
+ HypOkalemia.
This could be due to: Sepsis or DKA or others.
What to give?
→ IV fluids (0.9% Sodium chloride + Potassium chloride)
N.B. Do not give Sodium chloride alone (this won’t correct the low K+).
N.B. Do not give Dextrose (as the patient might already have high glucose
due to DKA)
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Hypothyroidism: Dry skin,
lethargy, tiredness,
weight gain,
intolerance to
cold, amenorrhea
or oligomenorrhea…etc.
In autoimmune hypothyroidism (Hashimoto’s thyroiditis), the patient may
have an associated autoimmune disease
such as Vitiligo,
ADDISON’S disease,
Pernicious Anemia,
DM type 1.
Sometimes, Hashimoto thyroiditis is given in the options instead of
hypothyroidism.
Pick it if the features are suggestive.
E.g., lethargy, fatigue, cold intolerance, dry skin, ↑TSH, ↓ free T4.
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101
102
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Prolactinoma
Micro and macroadenoma
Prolactinoma (↑↑ prolactin) due to pituitary adenoma
√ Prolactinomas are a type of pituitary adenoma, a benign tumour of the
pituitary gland.
√ The major effect of prolactinoma is decreased levels of some sex
hormones:
estrogen in women and testosterone in men.
◙ Pituitary adenomas can be classified according to:
√ Size (a microadenoma is <1cm and a macroadenoma is >1cm).
√ Hormonal status (a secretory/functioning adenoma produces and excess
of a particular hormone and
a non-secretory/functioning adenoma does
not produce a hormone to excess).
Prolactinomas are the most common type and they produce an excess of
prolactin.
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Congenital hypothyroidism
An infant with: prolonged neonatal jaundice (
or FHx of prolonged neonatal
jaundice),
Constipation,
dry skin,
FTT (Failure to Thrive),
Protruded tongue,
flat nose,
widely set eyes
→ Congenital Hypothyroidism.
N.B. This is very rarely seen nowadays because screening for
hypothyroidism
is available early after birth by measuring TSH from the
initial dried blood spot throughout the UK.
105
Stress hyperglycemia can occur after surgery or infection or trauma e.g.
RTA.
Do Fasting blood glucose when glycosuria subsides as a follow up
investigation.
106
Stress hyperglycemia:
√ After surgery,
stress, infections, trauma
→ high cortisol
→ high glucose
→ glycosuria (glucose in urine)
√ This subsides on its own in a few days.
◙ What to do next as a follow up step?
→ FASTING blood glucose (although it is a normal phenomenon, we need
to make sure of our diagnosis of the Stress hyperglycemia).
◙ What to do to know if it is DM or Stress hyperglycemia?
→ HbA1c “glycosylated haemoglobin”
As it reflects the blood glucose over the previous 3 months.
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Hypothyroidism causes
Hypothyroidism commonest causes:
• In the UK → Autoimmune (Hashimoto’s thyroiditis).
• Outside the UK -worldwide- → Iodine Deficiency. (Nutritional cause).
108
Cushing syndrome
A child who is obese, short, with abdominal striae with Hx of renal
transplant.
The likely cause of these features → (High Cortisol levels)
due to exogenous intake of steroids post renal
transplant.
The child is short because steroids are Anti-Vit D.
Also, high cortisol leads to
high blood glucose
which inhibits GH (growth hormone).
↑ Cortisol → ↑ Glucose → ↓ Growth hormone
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Thyrotoxicosis
The manifestations of thyrotoxicosis
(tremors,
anxiety,
wt loss,
tachycardia)
are physio-pathologically due to
→ High Metabolic Rate
110
111
112
Features of excess prolactin and diagnosis
◙ Features of excess prolactin:
• Men:
impotence,
loss of libido,
galactorrhoea
• Women:
amenorrhoea,
infertility,
galactorrhoea,
osteoporosis
◙ Diagnosis:
• serum prolactin (Normally below 400), if ≥ 5000, then suspect
Macroadenoma (prolactinoma).
• If > 2000, keep prolactinoma (even if Microadenoma) in mind.
• Others are low (
FSH, LH, Oestradiol)
• Confirmatory test: MRI Brain. √
113
◙ Prolactinoma Management:
Pituitary macroadenoma +↑serum prolactin (± amenorrhea):
√ First line: Dopamine agonist (
e.g., Cabergoline, Bromocriptine). They
inhibit the release of prolactin from the pituitary gland.
Important: If you have to choose between these 2 dopamine agonists, pick
→(Cabergoline) as it is 1st line and has higher efficacy and less side effects.
114
If no response to first line treatment for prolactinoma
??
If no response (ie, if these medications did not shrink the tumour and there
is still hyperprolactinemia) → switch to the second line.
to surgically resect and remove the
prolactinoma – the tumour- of the pituitary gland. (
If medical therapy
Trans-sphenoidal surgery failed).
• Note that: local manifestations caused by prolactinoma compressing
the surrounding structures may include:
→ progressively worsening headaches, visual disturbance.
• N.B. Cabergoline is more effective than Bromocriptine in normalizing
prolactin in Microprolactinoma.
• Other manifestations of hyperprolactinemia:
→ Galactorrhea,
Amenorrhea
or Oligomenorrhea,
Headaches,
Infertility,
Visual disturbances;
Bitemporal Hemianopias.
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Diabetic Neuropathy:
A diabetic patient with poorly controlled hyperglycemia:
- Loss of sensation (fine touch and pain) starts in toes bilaterally and
ascends (gloves and stocking pattern).
- Loss of Ankle jerk reflex bilaterally.
Mechanism: Microvascular injury → Damage of nerves.
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DKA (Diabetic KetoAciosis)
Q) First immediate management?
→ IV fluids followed by IV infusion of regular Insulin
The initial fluid therapy in a patient with diabetic ketoacidosis is:
“bolus”.
→ 500 ml of 0.9% sodium chloride over 15 minutes.
Followed by a continuous rate “infusion”:
◙ Features:
Fruity smell breath (pearl drops),
Abdominal pain,
Nausea and Vomiting.
pH < 7.3 //
Blood glucose > 12
or a known diabetic
// Bicarb < 15 //
Ketonemia > 3 or Ketone bodies in urine dipstick ++
N.B. When blood glucose reaches below 12,
shift IVF NS to 5% dextrose
to
avoid hypoglycemia (due to rapid correction of the hyperglycemia).
N.B. Hypokalemia may need to be corrected with KCl (Potassium Chloride)
after giving the first litre of IV normal saline.
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Conns hyperaldosteronism
Hypokalemia + Hypertension → Think of Conn’s syndrome
(hyperaldosteronism).
Therefore, the first hormone level to order is
→ Aldosterone.
As for the treatment:
Give surgery (Adrenalectomy).
120
In prolactinoma (pituitary adenoma) → (Hyperprolactinemia) →
Amenorrhea,
Galactorrhea →
Start drug therapy before surgery →
Dopamine Agonists (e.g. Cabergoline, Bromocriptine).
If no response → Transsphenoidal surgery to remove the pituitary adenoma.
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DM type 2 in an Obese (BMI > 30) patient without significant renal
impairment (eGFR above 45)
→ Start with Biguanide (metformin =
Glucophage).
• N.B. (SPR) cause weight gain
Sulphonylureas (e.g. Glibenclamide, Gliclazide),
Pioglitazones
(Glitazones)
and Repaglinide → Weight gain.
• As long as G FR is acceptable, the preferred option → Biguanide
(metformin).
Other cases:
- Obesity only → Biguanide (Metformin)
- Obesity + Significantly impaired kidneys
→ DDP-4 inhibitors (Gliptins), if
no response → Insulin.
- Impaired kidneys alone
→DDP4-inhibitors (Gliptins e.g., Linagliptin, Sitagliptin) or
Repaglinide or
Pioglitazone.
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DM type 2 medication if the patient is obese and eGFR < 30
and lifestyle
modifications have been tried and FBG is still above 11.1:
• Metformin? NO! metformin is contraindicated if GFR < 30
• Sulphonylureas? NO! it causes weight gain and the patient is already
Obese. Plus, in renal impairment, sulphonylureas have a higher risk to
cause hypoglycemia.
• Low sugar diet? No! Lifestyle modifications have already been tried
without benefits.
• DDP-4 inhibitors (Gliptins)? YES! They Do not affect weigh
and they
are safe in patients with renal impairment.
- N.B. Avoid DDP-4 inhibitors in HF and pancreatitis.
124
• Remember that:
√ ACE inhibitors (e.g., Ramipril
) and
√ Potassium sparing diuretics (e.g., Spironolactone)
can cause → hyperkalemia.
• Mild hyperkalemia (5.5-5.9)
• Moderate: (6-6.4)
• Severe (> 6.5)
- If mild hyperkalemia, no abnormalities on ECG, then the best initial step
(e.g. ACEi,
→ Stop the medications causing hyperkalemia Spironolactone
- If moderate, severe, and/or ECG changes: Tall Tented T wave, we
firstly need to protect the cardiac membrane from possible fatal
arrhythmia → or IV. Calcium gluconate or calcium chloride
- After that, OR even nebulized Salbutamol can be
given to shift the potassium intracellularly.
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PHEochromocytoma:
Excess catecholamines (adrenaline and noradrenaline) due to adrenal
adenoma
.
• P → Palpitations
• H → Headache, Hypertension
• Ph → Flushing (sweating)
• E → Episodic (Paroxysmal).
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