Endocrinology Flashcards
Cervical Cancer Risk Factors
HPV 16/18/33
16 activate Oncogene E6 –> inhibit p53
17 activate Oncogene E7
—> inhibit RB
Hypocalcemia Aetiology (Remember Note ?)
Hypoparathyroidism (Post Thyroidectomy/
Secondary HyperParaThyroidism
Malnutrition/CKD (Why?)
Medications Mnemonic is
Calcium Prevent Bone
Breakdown
Calcitonin
Bisphosphonates
Phenytoin Phenobarbital
Rifampicin / Clindamycin
Hypomagnesemia (Long Term PPI)
Respiratory Alkalosis
Psuedohypocalcemia due to
Hypocalcemia Features SPASMODIC Mnemonic
Spasms (Carpopedal - Trousseau sign)
Perioral Paranesthesia
Anxious
Muscle Tone High - Wheeze Dysphagia
Orientation
Dermatitis Herpetiformis
Chvostek Sign
Hypocalcemia Management
10ml 10% over 10 mins
Calcium Gluconate
Calcium Chloride Causes irritation
Hypercalcemia Causes
High-Normal or Elevated PTH (PTH-Dependent):
- Urinary Calcium > 250 mg/24 hr: 1ry & 3ry Hyperparathyroidism
- Urinary Calcium < 100 mg/24 hr: Familial Hypocalciuric Hypercalcemia
Suppressed PTH
(PTH-Independent):
Measure PTHrP – (25-OH D) – (1,25- OH D) -
- Elevated PTHrP: Squamous Cell Cancer
- Elevated 1,25(OH)2D: Check for Lymphoma or Sarcoidosis (Chest X-ray)
3.. Elevated 25(OH)D: Vitamin D Toxicity
Normal Results
o Hyperthyroidism
o Multiple Myeloma
o Adrenal Tumor
o Acromegaly
o Vitamin A Toxicity
o Immobilization
o Milk-Alkali Syndrome
o Medications (e.g., Thiazide Diuretics, Lithium, Theophylline, Calcium Containing Antacids )
Review T2DM Management (Note)
Side Effect of GLP1 Mimetic (-TIDE)
Nausea and Vomiting
Which Oral Antidiabetic Drug causes increase in incretins ? and HOW ?
DDP4i
By decreasing their breakdown peripherally
Thyroid Cancers
Types and FACTS !!!
Papillary
Lymphatic Spread Predominates
Follicular
Medullary
1.Cancer of Parafollicular C cells derived from NEURAL CREST not Thyroid
2. Elevated Calcitonin Levels
3. Hematogenous and Lymphatic Spread
Anaplastic (Treatment Resistance (Chemo Ineffective) and PRESSURE Sx)
Lymphoma (Associated with Hashimoto’s)
Management of papillary and follicular cancer
Thyroidectomy
Iodine to kill of residual cells
Yearly Thyroglobulin
What HLA is Graves ? and What Hypersensitivity ?
HLA DR3 and HLA DRB8
Pathophysiology behind Graves Opthalmopathy ?
Autoantibodies activate Retro-orbital T cells –> Secrete IFN Gamma and TNF Alpha –> Active Fibroblast —> GAG accumulate –> Increase Adiposity –> Muscle Inflammation
De Quervains Thyroiditis
Treatment and Radioactive Scan
Self Limiting and Naproxen
Steroids if become Hypothyroid
globally reduced Radioactive Uptake
Drugs Causing Hyperthyroidism ?
Amiodarone
IL2
Lithium
Tyrosine Kinase Inhibitors
Alpha Interferons
Jade Bosedow Phenomenon explain ?
Chronic Iodine Deficiency
Upregulation of Iodine Receptors
Excess Iodine via Contrast
Trigger Hyperthyroidism
Essentially Contrast Induced Hyperthyroidism
Wolf Chairkoff Phenomenon Explained
Sodium Iodine Sympoter in Basolateral Membrane gets downregulated with Exceeding High Levels of Iodine and this also downregulates TPO which would usually use the I- to made T3 and T4.
After 2 days the Chairkoff effect is turned off and the cells return to normal
But in Hashimoto’s there are less follicular cells and as such the WCE is turned off slower.
Histology for Hashimoto
Hurtle Cells
Lymphocytic Infiltration with Germinal Centres
Histology for DeQuervain Thyroiditis
Multinucleated Giant Cells and Granuloma
Histology for Riedel Thyroiditis
Dense White Fibrotic Tissue
Subclinical Hypothyroidism Treatmen t
4-10 + Normal T4
<65 + Symptomatic –> Trial Levothyroxine –> 2 occasions 3 months apart NAD –> STOP
If >80 - Watch and Wait
> 10 + Normal T4
<70 - Start
>80 - Watch and Wait
ALL T4 and TSH must be on 2 occasions 3 months apart
ALSO
if asymptomatic people, observe and repeat thyroid function in 6 months
Euthyroid Sick Syndrome
Low T3 Syndrome -
T4 and TSH - NAD
Total and Free T3 Low
rT3 High
Low T3 and Low T4 Syndrome
T4 / TSH / T3 Low
rT3 High
MEN 1 2A and 2B
Men 2A PPM
Medullary (RET)
Primary Hyper Para
Phaeochromocytoma
Men 1 PPP (MEN1 Oncogene)
Pancreatic Tumor (Insulinoma / Gastrinoma )
Pituitary Adenoma (Prolactinoma)
Parathyroid Hyperplasia
Men 2B PMM (RET)
Marfanoid
Medullary
Pheochromocytoma
Primary Hyperparathyroidism can PTH be inappropriately Normal ?
Yes !!!!
Treatment for Primary Hyperparathyroidism
If <0.25 than the Upper Limit + >50 + No End Organ Damage –> Conservative
If Unsuitable for Surgery – > cinacalcet (allosteric activation of calcium sensing receptors)
X ray findings for Primary Hyperparathyroidism ?
PepperPot Skull and osteitis fibrosa cystica
technetium-MIBI subtraction scan
Foods advised in Hyperkalemia
bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
Pre-diabetic and engaging in exercise but HbA1C rising. Would you add Metformin ?
YES !!!!
NICE recommend metformin for adults at high risk ‘whose blood glucose measure (fasting plasma glucose or HbA1c) shows they are still progressing towards type 2 diabetes, despite their participation in an intensive lifestyle-change programme’
Which RTA linked to Renal Stones and Sjogren Syndrome ?
Distal
Urine is also alkalinic !!!
Type 1 / 2 and 4 RTA
- Pathophysiology
- Urine pH and K
- Causes
Type 1 ( Distal )
Defective H+ secretion
pH<5.3 and HypoK
Associated with Nephrocalcinosis / RA / Sjogren / Analgesic Nephropathy
Type 2 ( Proximal )
Defective HCO3 reabsorption
pH initially >5.3 later <5.3 HypoK
Associated with Wilsons / Cystinosis / Carbonic Anhydrase Inhibitors / Amyloidosis / Outdated Tetracyclines /
Type 4
pH<5.3 HyperK
Diabetes / Hypoaldosteronism / Spirinolactone / NSAID’s / ACEi
Treatment for Types 1 2 and 4 RTA ?
1 = Potassium Citrate
2 = Potassium Citrate
4 = Fludrocortisone
Drugs Causing Gynecomastia
DISCO GF HAS Big Mouth
Digoxin
Isoniazid
Spironolactone
Cimitidine,Cannabis,CCBs
Oestrogen
Goserelin
Finasteroid
Heroin
Anabolic Steroids,AntidepreSsants
Busulfan
Methyldo
Bratter / Gitleman / Liddles
Fanconi syndrome - PCT
-type 2 renal tubular acidosis (normal AG)
-Genetic in proximal convoluted tubules (no reabsorption for glucose - amino acid - uric acid - phosphate - bicarbonate
(Rickets - osteomalacia) - met acidosis
Bratter syndrome ‘loop of henle’
Frusemide like
Hypocalcemia - magnesemia - kalemia
Without HTN
Hypercalcuria (dd with gitelman)
Gitelman syndrome ‘DCT’
Thiazide like
Hypokalemic metabolic alkalosis
No HTN
Hypocalcuria
Liddles syndrome ‘Collecting duct’ ‘AD’
-epithelial sodium channels in DCT
Hypokalemia due to Hyperaldosteronism - hypertension - metabolic alkalosis
Causes of Addisons Disease ?
Infection - TB (MCC)
Infiltrative - Amyloidosis , Sarcoidosis
Waterhouse Frederickson
CAH
Investigative Pathway for Cushings
REMEMBER and READ NOTES QUICK
MOA of Sulphonyl urea ?
Bind to K(ATP) channels on Beta Pancreatic Cells
Increase Pancreatic Insulin Secretion
Only works if adequate B cell reserve
MOA of Pioglitazone ?
Activation of peroxisome proliferator-activated receptor-gamma (PPAR gamma)
Pituitary Adenoma Treatment ?
If Non Functioning Adenomas causing Compressive Symptoms OR Generalized Hypopituitarism via compression –> Transsphenoidal Resection
If Prolactinoma (Prolactin Levels >100) then Cabergoline (Dopamine Agonist)
GH secreting then Somatostatin Analogues or GH Antagonist (pegvisomant)
If ACTH-secreting adenomas then Ketocanazole or Metyrapone or Neuromodulators like pasireotide
What Percentage is TSH Receptor Ab seen in Graves ?
90%
What Percentage is Eye Symptoms seen in Graves ?
30%
What Percentage of TPO seen in Graves ?
75%
Women with Premature Ovarian Failure Treatment ?
COCP or HRT until 51 years but need contraception in case spontaneous ovarian activity
Urge and Stress Incontinence Management
Urge
- Bladder Training (6 weeks)
- Oxybutynin
- Mirabegron
- If Nocturia - Add Desmopressin
- Urodynamic Studies showing Detrusor Overactivity –> Botox A
Stress
- Kegel Exercises (8 contractions performed 3 times per day for a minimum of 3 months)
2.Surgically -
Tape
Intra-sphincter Bulking Agents
Colposuspension - Duloxetine if Surgical Declines
Mirabegron CI when ?
Uncontrolled HTN
Pregnancy Thyroid Picture
Functional T3 and T4 NAD
But Total T3 and T4 RAISED due to Increased Thyroglobulin
Pregnancy when to Check Thyroid levels and how to adjust ?
thyrotrophin receptor stimulating antibodies should be checked at 30-36 weeks gestation
serum thyroid-stimulating hormone measured in each trimester and 6-8 weeks post-partum
4-6 weeks into pregnancy increase dose by 50%
How to change Metformin dose in Ramadan ?
What about Poiglitazone ?
Gliclazide ?
1/3 dose in the Morning
2/3 rd dose after Ifthar
Pioglitazone no changes
If BD Gliclazide then take larger portion after sunset
If OD then take after sunset
Insulin Stress Test needed for which condition ?
Panhypopituitarism
When not to use QRISK ?
T1DM
eGFR < 60 or albunminuria
Familial Hypercholesteremia
When to consider familial hypercholesteremia
Total Cholesterol >7.5 mmol/l
OR
Premature (<60) CVD in Index or First Degree Relative
When to give Statins in T1DM ?
atorvastatin 20 mg should be offered if type 1 diabetics who are:
> 40
Diabetes >10 years
Established nephropathy or
have other CVD risk factors
In CKD if the Non- HDL doesn’t reduce by 40% then what should be done ?
if eGFR > 30 increase dose
if eGFR < 30 Consult Renal
DVLA and Diabetes for Group 1 and Group 2 Vehicles
DVLA and Diabetes: Simplified for MRCP
Group 1 (Car/Motorcycle Drivers)
1. On Insulin:
- Allowed if:
- Full hypoglycaemic awareness.
- ≤1 severe hypoglycaemic episode needing help in the last 12 months.
- No visual impairment related to diabetes.
-
On Tablets (e.g., Sulfonylureas):
- No need to notify DVLA, unless:
- >1 severe hypoglycaemic episode in the last 12 months. -
Diet-Controlled Diabetes:
- No need to notify DVLA.
Group 2 (HGV/Bus Drivers)
1. Insulin or Hypoglycaemic Drugs (e.g., Sulfonylureas):
- Must meet all these criteria:
- No severe hypoglycaemia in the last 12 months.
- Full hypoglycaemic awareness.
- Regular blood glucose monitoring:
- Twice daily and before driving.
- Use a memory-function meter (records readings for ≥3 months).
- Understands risks of hypoglycaemia.
- No diabetes-related complications that impair driving.
-
Practical Step:
- Complete VDIAB1I form for application.
Key Tip to Remember
- Group 1: Rules focus on awareness, episodes, and vision.
- Group 2: Stricter with no episodes, monitoring, and complication-free criteria.
What test is used to Confirm Acromegaly ?
First Raised IGF1
Then OGTT and Serial GH Suppression to Confirm
How does Alcohol cause exaggerated Insulin Secretion ?
Alcohol affect pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion
Hypertension + Hypokalemia
Hypokalemia with alkalosis==> Cushing’s, Conn’s, thiazide n loop, vomiting
Hypokalemia with acidosis==> Diarrhea, RTA, Acetazolamide, Partially rx dka
Hypokalemia with Hypertension==> Cushing’s, Con’s, Liddle’s,11-beta hydroxylase deficiency
Hypokalemia without Hypertension: ==> Diuretics, RTA 1 n 2, Barterr’s, giteLman’s and GI loss
Whats the Rescue Drug for Neuropathic Pain ?
Tramadol
Type 4 RTA Pathophysiology ?
Hypoaldosteronism
at DCT
Thiazolidinediones
increased risk of fractures
Liver Derangement
MOA of Orlisat ?
Pancreatic Lipase Inhibitor
BMI of 28 kg/m^2 or more with associated risk factors
BMI of 30 kg/m^2 or more
continued weight loss e.g. 5% at 3 months
orlistat is normally used for < 1 year
Pretibial Myxedema Associated with Hypothyroidism ?
NO !!!!
Pretibial myxoedema = thyrotoxicosis
Myxedema coma = severe HYPOthyroid
KlineFelters Syndrome vs Kallmann Syndrome
Kallmans- hyPOgonadotropic hyPOgonadism
Klinefelters- HyPERgonado. hyPOgonad
Klinefelters = Tall, titties, tiny testes, high gonad hormones
Kallman’s = 1 ball and tall, can’t smell at all, normal/low hormones (gonado trophic)
Diabetes Facts about Inheritance
HLA DR4 > HLA DR3 in T1
Polygenic Inheritance ( TCF7L2 is the most powerful )
Identical twins show a genetic concordance of 40% in T1 and 100% in T2
Criteria for Parathyroidectomy
Make an incision ACROSS parathyroid when
Age <50
Calcium (0.25 above normal)
Renal failure (gfr<60)
Osteoporosis or FF
Stones
Symptomatic
Familial Hypercholesteremia
- Inheritance
- When to consider a diagnosis of FH
- Diagnostic Criteria
- Management
- Autosomal Dominant
If
a. Total Cholesterol > 7.5
b. Premature (<60) CVD in Patient or 1st Degree Relative
Children need screening
c. At 10 if one parent Affected with FH
d. At 5 is both parent affected
- Simone Brookes Criteria
Total Cholesterol >7.5 AND LDL-C >4.9
PLUS
Definite - Tendon Xanthomata in Patient 1st or 2nd Degree Relative OR DNA evidence
Possible -
a. 2nd Degree Relative MI <50
b. 1st Degree Relative MI
<60
c. Family History of High Cholesterol
- High Dose Statins
Screening of Family Members and Children
Statins stopped 3 months before conception
What is the Clinical Dx for FH (Homozygous) ?
Adults (>15):
LDL-C >13
Children (<10) /young people (10-15):
LDL-C >11
Primary Prevention in
T1DM
T2DM
CKD
Creatinine Kinase and LFT Criteria for Statins
Creatinine
If CK >5x upper limit of normal, remeasure CK after 7 days
If CK still >5x upper limit of normal, do NOT start statin
If CK raise but <5x, start lower dose statin
LFT
Before start: measure LFT as baseline
At 3 months, 12 months
If LFT >3x upper limit of normal, do NOT give statin
Gestational Diabetes
Screening and Treatment
5678
Joint Diabetes and Antenatal Clinic in 1 week
if FPG<7 –> Trial Diet
a. After 1/2 weeks if not met –> Metformin
b. If still not met –> add SHORT ACTING insulin
If FPG > 7 —> Insulin
If 6-6.9 + Complications (Macrosomia/Hydramnios) —> Insulin
If decline insulin then Glibenclamide
Gestational Diabetes
Risk Factors and When to Screen
- BMI of > 30 kg/m²
- previous macrosomic baby weighing 4.5 kg or above
- previous gestational diabetes
- first-degree relative with diabetes
- family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle Eastern)
- unexplained stillbirth in a previous pregnancy
If Previous GDM then Screen at Booking AND 26-28 weeks
If Other RF then Screen at 26-28 ONLY
Things to do if Pre existing Diabetes gets Pregnant
- Weight loss for women with BMI of > 27 kg/m^2
- stop oral hypoglycaemic agents, apart from metformin, and commence insulin
- folic acid 5 mg/day from pre-conception to 12 weeks gestation
- detailed anomaly scan at 20 weeks including four-chamber view of the heart and outflow tracts
- tight glycaemic control reduces complication rates
6.treat retinopathy as can worsen during pregnancy
Fibrates MOA ?
Activating PPAR alpha receptors –> Increasing LPL –> Decreasing Triglyceride
Also ezetimibe decrease intestinal absorption of Cholesterol
Fibrates Side Effect
GI and VTE
How many hours after should Iron be given after Thyroxine ?
4 hours
Check Thyroxine Levels after 8-12 weeks when starting or dose adjusted
Diagnostic Pathway for Diabetes
Ketones Positive + Weight Loss = T1DM
If NO , Autoantibodies + = LADA
If NO , Non Obese and <25 = MODY
If NO , T2DM
LADA Features
β-islet autoantibodies: GAD, Tyrosine phosphatase (IA2)
Mid 30s , Rapid Weight Loss and NOT RESPONDING TO ANTI DIABETICS
MODY
- Inheritance
Autosomal Dominant with
1. 63% transcription factors (HNFα1, HNFα4, HNF1β)
2. 37% glucokinase mutations
MODY 3 (MCC) –> HNF⍺1 gene –> HCC –> Give Sulphonylureas –> Commonly develop Complications of Diabetes
MODY 2 - Glucokinase Deficiency –> Rarely develop complications of Diabetes
MODY 5 –> HNF1β gene –> Liver and Renal Cyst –> Insulin
MODY1 (HNF4A)
HRT increases risk of which Cancer ?
If Progesterone –> Breast
If Estrogen –> Endometrial
Never give Estrogen to women with Hysterectomy
What’s the Equation to Calculate Average Blood Glucose from HbA1C
(2*HbA1c in %) - 4.5
Which Conditions cause a Falsely Elevated Increase in HbA1c vs Falsely Low ?
Falsely High (Longer RBC Life Span)
Vit B12 Def / Iron Def / Splenectomy
Falsely Low
Hemolytic Conditions
Types of Dyslipidemias
Inheritance Patterns
Type 1 (AR): elevated chylomicron, defective lipoprotein lipase
Type 2 (AD): elevated cholesterol (LDL+/-VLDL), defective LDL receptor/ ApoB100
Type 3 (AR): elevated cholesterol + triglycerides, defective ApoE
Type 4 (AD): elevated triglycerides, increased hepatic production + defective lipoprotein lipase
odd numbers = AR, even numbers = AD
from 1-4 to remember what’s elevated, if you say chylo, chole, mixed, trigs, it kinda rhymes
Eruptive xanthoma»_space; Type 1 (Hypertriglyceridemia)
Tendon xanthoma»_space; Type 2 (Familial hypercholesterolemia)
Tuberous/Palmar xanthoma»_space; Type 3 (Remnant hyperlipidemia)
Barters Disease Pathophysiology
Defective NKCC2 channel in the ascending loop of Henle
Drugs causing SIADH Mnemonic ?
SSRI
Indomethacin (NSAID)
Antidepressants (TCA)
Diuretics (Thiazide)
Haloperidol
Cannot – Cyclophosphamide, Carbamezepine
Void - Vincristine , Vasopressin
Hyponatremia Causing Drugs ABCDEFG
ACEi/AntiPsychotics/ AntiDepressants
Carbamezepine
Desmopresin / Diuretics
Ethosuximide
Furosemide
Glicazide
Heparin
Galactosemia Features
Features
Jaundice
Failure to thrive
Hepatomegaly
Cataracts
Hypoglycaemia after exposure to galactose
Fanconi syndrome
Galactosemia Pathophysiology
Absence of galactose-1-phosphate uridyl transferase
Intracellular Accumulation of Galactose-1-Phosphate
Autosomal RECESSIVE
Thyroid Storm Management
Propranol
PTU>Carbimazole
IV Hydrocortisone
Lugols Iodine (given 1 hour after PTU)
Hyponatremia when to give Bolus Hypertonic vs When to give Hypertonic Infusion
Na less than 120 hypertonic saline bolus
Na 120 to 129 hypertonic saline infusion
Na 130 to 135 0.9% NaCl
Acute Hyponatremia < 2 days give BOLUS
Chronic Give Infusion
Read below for explanation
it’s all about acute vs chronic. if its definitely acute (<2 days) hyponatraemia you can treat it as quick as possible as your brain has not adjusted to the low sodium, in acute your brain is swelling (causing seizures etc) and will swell until it herniates thats why its important you correct it asap. the classic example is the marathon runner who for 24h after the marathon drinks loads of water and then has a fit and collapses, this is because their sodium went from 140 to 110 so fast they get cerebral oedema - if you correct it too slowly the oedema will kill you rather than the any CPM. it’s in chronic hyponatraemia you can’t correct it too quickly becuase the brain isnt swollen as it has adjusted to the low sodium so you are at risk of CPM. this is why the first point in the explanation is acute vs chronic - changes everything.
However if you don’t know if it’s acute or chronic then treat as chronic as it’s more likely. With the marathon runner it’s pretty clear it’s acute but the biddy in the resi home… less so. It’s chronic hyponatraemia you look at the volume status and refer them to someone smarter than you
How does Thyroid Metabolism Happen ?
Iodide taken up by Na/I- transporter
- OXIDIZED into I2
- Tyrosine is bound to Thyroglobulin (lets call this TG)
I2+ TG = DIT
I + TG = MIT
This is ORGANIFICATION
DIT and MIT is endocytosed - COUPLING
DIT + DIT = T4 (Most Abundant)
MIT + DIT = T3 (Most Active)
THYROIPERIOXIDASE is the ENZYME CATALYSING ORGANIFICATION , COUPLING and OXIDIZATION
MOA of PTU ?
Inhibit De- Iodinase
Which Peripherally Converts T4 to T3
MOA of DPP4i ?
Inhibit breakdown of Incretins like GLP-1
Explain SIADH Pathophysiology
What cancer are patients with Acromegaly Prone to have ?
Colorectal Cancer
PCOS Pathophysiology Explain
Pendred Syndrome
Euthyroid
Goitre
Autosomal Recessive
Slow Academic Progress
Sensineural Hearing Loss (worsened by head trauma)
Classic 1.5 cochlear turns vs the normal 2
Primary Hypoparathyroidism vs
Pseudohypoparathyroidism vs Psuedopsuedohypoparathyrodism
Primary HypoParathyroidim
Low PTH
Low Calcium and High PO4
Peudohypoparathyroidism (PTH receptor resistance)
so High PTH
but Low Ca and High PO4
PsuedoPsuedoHypoparathyroidism
(All Biochemistry Normal but behaves like Pseudo - No receptor resistance)
Pseudo and Pseudo Pseudo
1. 4th and 5th Short Metacarpal (Knuckle Knuckle Dimple Dimple) vs Turners only 4th Metacarpal Short (Knuckle Knuckle Dimple Knuckle)
2. Short Stature
3. Low IQ
How do diagnose Pseudo Hypoparthyroidsm
Ellsworth Howard Test
give PTH infusion
pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.
in Pseudo Pseudo Urinary cAMP rises as normal
Pseudo and Pseudo Pseudo part of what of what syndrome ?
Albright Hereditary Osteodystrophy
What drug given together with Pioglitazone will cause more Peripheral Edema
Insulin
Pioglitazone Side Effects
Pioglitazone and the ‘URES’
heart failURE
fractURE
bladdURE
GLP 1 Actions
Increase Insulin
And
Decrease Glucagon
Congenital Adrenal Hyperplasia Pathophysiology
3 Enzymes
- 21 Hydroxylase –> Aldosterone Synthesis (SALT)
- 11 beta Hydroxylase –> Cortisol (SALT)
- 17 alpha Hydroxylase
–>Testosterone (SEX)
If on Pathway is blocked then the resources are shifted to the other pathways
So in 21 Hydroxylase Deficiency -
Virilization and Male Precocious Puberty or Female Ambigous Genetalia AND HYPOTENSION from lack of Aldosterone
11 beta hydroxylase there is HYPERTENSION with Virrilization because 11 beta is one step below the 21 hydroxylase as such elevated levels of DEOXYCORTISTERONE which is a weak mineralocorticoid. (LOOK AT THE PATHWAY TO UNDERSTAND)
In 17 Alpha Hydroxylase Deficiency –> Less Testosterone and Less Cortisol but MORE ALDOSTERONE –> Feminized Mae Gentalia and HYPERTENSION
https://www.youtube.com/watch?v=SLgWDg36u74f
Hungry Bone Syndrome
Post Op Sudden Decrease in PTH and Calcium Acutely
Osteoclasts have been used to demineralizing and when the Parathyroid Gland is removed BONES REMINERALISE RAPIDLY and bring Calcium Down
Insulinoma Investigation and Treatment ?
Supervised Fasting upto 72 hours
Dioxide and Somatostatin if patients not candidates for surgery
Side Effect of Glucocorticoids
S.E of corticosteroids – GLUCOCORTICOIDS
G – ^ Glucose – DM like state
L - ^ Lipids – hyperlipidaemia
U – Ulcers – peptic ulcers
C – Cushing’s (Moon ace + buffalo hump + striate)
O – Obesity
C – Children – Growth suppression
O – Osteoporosis & Avascular Necrosis of bone
R – Retention of fluid (Edema & HTN )
T – Thinning of Limbs > myopathy
I – Immuno-suppression (^ Infection)
(but also causes Neutrophilia)
C – Catract
O - Open angle glaucoma
I – insomnia
D – Depression & Psychosis
S – Suppression of Endogenous Cortisol > may precipitate Addison’s on abrupt cessation of Tx
Drug Induced Rash in Steroids Appearance
monomorphic papular rash without comedones or cysts.
This does not respond to acne treatment but improves on drug discontinuation
Hypothyroidism is linked to Dyslipidemia
Hyperthyroidism to Oligomenorrhea
Hypothyroidism is Menorrhagia
Barters defective in what site and which Protein ?
NCCK2 channels at the Thick Ascending Loop of Henle
Liddle - Continuous activation of ENAC at Collecting Duct so give Amiloride
Gittleman is defective sodium-chloride co-transporter in the distal tubule like the mechanism of action of thiazide
Kallmann Syndrome vs Kline Felters
Small Atrophied Testis (Klinefelter’s) vs Cryptorchidism (Kallmann)
In KALLMANN
‘delayed puberty’
hypogonadism
cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above-average height
KALLMAN FSH AND LH low (TALLMAN but OPPOSITE)
KLINEFELTER’s HIGH FSH AND LH
Pathophysiology of PCOS
Theca Cells
Cholesterol —> Androgens
No Aromatase to convert into EstroDIOL
Stimulated by LH
Granulosa Cells
Androgens —> EstraDIOL (E2) via Aromatase
Stimulated by FSH
No Ovulation
No Corpus Luteum
No Progesterone
No inhibition of GnRH
Increased Pulsatile GnRH –> Increase LH > FSH
LH –> Increase Aromatization –> Hyperandrogenism
Low FSH —> unable to ovulate —> Infertility
Insulin stimulates androgen synthesis in Theca Cells and Adrenal Cortex —> Negative Feedback into Pituitary —> Causing more LH/FSH imbalance + also DECREASES insulin sensitivity —> Pancreas Releases More
So Metformin increases insulin sensitivity and decreases gluconeogenesis
Remember Primary Hyperparathyroidism
PTH can be NORMAL
Chronic Alcoholic Patients who have Hypoglycemia How do you Treat ?
IV Dextrose
NOT IM Glucagon because less Glycogen stores !!!!
Insulinoma is Whipples Triad Classically
1) Symptoms of Hypoglycemia (sweating, EARLY MORNING double vision)
2) At times when Glucose Conc is low
3) Resolved by eating
Insulinoma DIAGNOSED with ______
Supervised Fasting
What is used to differential between Pseudo Cushing and True Cushing’s ?
Insulin Stress Test
Biggest Complication of Thyroid eye Disease
Exposure Keratinopathy
Sick Euthyroid Syndrome Pattern
TSH normal / low; Thyroxine low
T3 low.
A normal short synacthen test does not exclude adrenocortical insufficiency due to ______________________
pituitary failure
What drug is given before Transsphenoidal Surgery in Acromegaly
Octreotide
