0% found this document useful (0 votes)
65 views67 pages

Endocrinology Blank

The document is a comprehensive endocrinology workbook authored by Dr. Priyansh Jain, covering various topics including diabetes pathogenesis, thyroid physiology, adrenal gland disorders, and parathyroid pathology. It provides detailed insights into the diagnosis, complications, and management of endocrine diseases, alongside summaries for each chapter. The workbook serves as a resource for medical education, particularly in understanding the complexities of endocrinology.

Uploaded by

6xscscz5ks
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
65 views67 pages

Endocrinology Blank

The document is a comprehensive endocrinology workbook authored by Dr. Priyansh Jain, covering various topics including diabetes pathogenesis, thyroid physiology, adrenal gland disorders, and parathyroid pathology. It provides detailed insights into the diagnosis, complications, and management of endocrine diseases, alongside summaries for each chapter. The workbook serves as a resource for medical education, particularly in understanding the complexities of endocrinology.

Uploaded by

6xscscz5ks
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 67

ENDOCRINOLOGY

WORKBOOK
By
Dr. Priyansh Jain

RISE WITH ARISE


ARISE MEDICAL ACADEMY
https://instagram.com/arisemedicalacademy
www.arisemedicalacademy.com
INDEX
1. Pathogenesis of diabetes
2. Diabetes - presentation, diagnosis & complication
3. DKA & HHS
4. Thyroid physiology
5. Interpretation of thyroid profile test
6. Hypothyroidism & Hyperthyroidism
7. Thyroid disorders
8. Adrenal gland physiology
9. Hyperaldosteronism
10. Cushing sundrome
11. Pheochromocytoma
12 . Adrenal insufficiency
13. Parathyroid gland - physiology
14 parathyroid gland - pathology
15. Pituitory glamd - physiology
16. Pituitory disorders
17. Endocrine neoplasia
Chapter 1
Pathogenesis of Diabetes mellitus

PATHOGENESIS OF TYPE 1 DM

Relation of Insulin with body weight

Occur at Age-
B- cell mass at the time of diagnosis-
Concordance in identical twins -
body wt
PATHOGENESIS OF TYPE 2 DM

B-cell

Glut-2

Blood

S.muscle
Body wt

PATHOGENESIS OF TYPE 1.5 DM


LADA -LATENT AUTOIMMUNE DIABETES OF ADULTS

PATHOGENESIS OF Maturity onset of diabetes (MODY)

M
GLUT 2

HNF-1-ALPHA

Endoplasic reticulum

B-cell
CaLcium channel

Inheritance pattern -
So
Types. Of MODY
Age of onset -
B-cell mass-

Rx-

BRONZE DIABETES
Caused by -

Iron deposition - skin


- liver
- pancreas

So manifest as
Type 3 Diabetes

Summary

Type Of DM Pathogenesis
1
1.5
2
Mody
Bronze

Overall M/C type of DM -


Overall most rare type of DM-

Also know
Gene associated with insulin production - CTL4A
chromosome for MODY type 3- chromosome 12
Chapter 2
Diabetes Presentation , diagnosis and Complications

C/f

Diagnosis
Pre-diabetes
Normal Impaired glucose Diabete
tolerance
Fasting
Post prandial
HbA1C
Random

Post prandial means -


Best test for

HbA1C
Sugar level Sugar level
95 mg/dl 95 mg/dl

Hb - 15 gm/dl Hb - 5 gm/dl

Glycated albumin ( s. Fructosamine ) -

Shows average blood sugar of -

Oral glucose tolerance test (OGTT)

4pm 6pm

Extra point
Healthy So

4pm 6pm

DM So

4pm 6pm
Mechanism for Fasting hyperglycemia
healthy Meal
Fasting sugar at 8am

DM

Fasting sugar at 8am


7pm

Mechanism for Post prandial hyperglycemia.


healthy Meal

DM
Meal

Complication of DM

Myocardium

Brain
Earliest change Earliest change

Most specific change Most specific change

So retinal examination in type 1 DM.........................


and type 2 DM .............
Managment of DM

1- BIGUANIDES

MOA
Effect on Hb1aC
S/E -
C/I

2 - sulfonylurea - 1st generation


2nd generation

MOA
S/E
MOST POTENT

3- SGLT -2 inhibitors

SGLT2

Eg-
S/E
Preferred in

4 thiazolidinediones
MOA
S/E
5.Incretins

GLP(glucagon like peptide -1 ) analogue -


MOA
S/E-

DPP-4 INHIBITOR-

Most renal safe DPP-4 #-

6. Alpha- glucosidase inhibitor


Complex carbohydrate

Glucose
Other
Carbohydrate

Glucosidase
7. Amylin analogue

Gastric emptying

8.insulin

Basal insulin

Prandial insulin

Complication of insulin therapy

DAWN phenomenon

Gloucose
Level
Somogyi phenomenon

So in
Type 1 DM
Type 1.5 DM
Type 2 -

MODY

Summary
*Hb1ac shows average of - ........................weeks

2. Anemia leads to fasle ............ HB1ac

3. FALSE + OGTT --

4. FALSE - ve OGTT -

5. Fasting hyperglycemia in DM is due to ........

6.anti - diabetic to avoid


If -- DM + HF
-- DM + medullary ca of thyroid
-- DM + uti
-- DM +MI
7. Maximum Hb1AC reduction -
8. Longest acting insulin -
9. Dawn phenomenon - fasting .................................. Rx-
10. Somogyi phenomenon - fasting ........................... Rx-

Chapter 3
Diabetic keto acidosis (DKA) &
Hyperglycemic Hyperosmolar State (HHS)

DIABETIC KETO ACIDOSIS

Pathogensis
B- cell
Fatty acid

Blood
glucose

Tissue
C/f-

Investigation - blood glucose level-


- urine keton
- ABG - pH-
- S. Na+

Rx-

Complication

Initially Later

Hyperglycemic hyperosmolor state

Commonly seen with -

Age -
Pathogenesis

Blood osmolarity

Blood

C/f

Treatment
Summary
1. DKA commonly seen with type ...... DM and trigger is ......................../,..........,.....

2. M/C keton body synthesized in liver is -

3. Keton body having fruity smell-

4. Keton body can be detected by -

5. Main stay of rx in DKA-

6. ............................... insulin used in DKA managment .

7. MCC of death in DKA is .............

8. HHS seen with type .... DM in ..................... age group .

9. C/f of HHS - commonly - ...................................t manifestation .

10 . prognosis of HHS
Chapter 4
Thyroid Physiology

Thyroid gland

Cancer of parafollicular c cell is called

Pituitary
T4 v/s T3

Production
Activity
Half life

Convertion of T4 To T3
Brain

Effect of thyroxine
On α recpetor
On B- receptor
Metabolism
Bone
Testosteron

Thyroid FeedbBack system

Hypothalamus

Pituitary
Chapter 5
Interpretation of thyroid profile test

Hypothalamus

Pituitary

Hypothalamus

Pituitary

Hypothalamus

Pituitary
Hypothalamus

Pituitary

Hypothalamus

Pituitary

Lets practice
T4 TSH Diagnosis

Primary hyperthyroidism

Sick euthyroid syn


Chapter 6
Hypothyroidism & Hyperthyroidism
Hypothyroidism
Etiology

C/f. - Metabolism
Lipid level
Hair
Eyebrow
Skin-
Deep tendon reflex
Heart (ECG)-
GIT -
body temprature-
Menstrual bleed-

Rx-
Hyperthyroidism

Etiology

C/f. - Metabolism-
Skin-
Deep tendon reflex -
Heart - HR ........./ SBP ......../ ......CMP/.......... .............. murmur
Hands-
GIT -
body temprature-
Menstrual bleed-
Upper eye lid sign of hyperthyroidism

Managment of hyperthyroidism

Follicular cell Colloid

So
1. Thyroid peroxidase inhibitor -
2. Harmone release inhibitor -
3. Peripheral convertion inhibitor-
Chapter 7
RAIU & Thyroid disorders
Radioactive iodine uptake test (RAIU)

For RAIU - ................... ...... is used.

Mechanism of RAIU -
Thyroid Pathology

Hashimoto thyroiditis

Pathogenesis

Thyroglobin (TG)

Thyroid peroxidase (TPO)

Associated with -

C/f - initially -
- later. Stage (main) -

Increased risk of -

Biopsy -

Rx-
Subacute thyroiditis or dequervein thyroiditis

Pathogenesis

C/F - initially
- later

Rx-

Reidel thyroiditis

Pathogenesis

C/f-

Associated with -

Rx - for hypothyroidism
- to decrease fibrosis-
Grave disease

Pathogenesis
Immune
Pituitary system

TSH receptor

Associated with-

Rx
Toxic multinodular goiter

Pathogenesis

C/f

Rx

Thyroid storm

Pathogensis

C/f - HR -
BP -
Body temp. - Sensorium -

Rx-

Myxedema coma

Pathogenesis

Poe
C/f - HR -
BP-
Body temp.-
Sensorium - S.glucose............. S.Na +..............

Rx-

Extra point - Wolf- chaikoff effect

Jod basedow effect


Summary
1. More active .......... form .
2.more production of .............. form.
3. Calcitonin is secreted by ..................................................cell.
4.MCC of hypothyroidism .........
5. DTR - In hypothyroidism ..........
- in hyperthyroidism..........
6.upper rim of sclera is visible is called as .................................. sign.
7.thyroid peroxidase inhibitor drugs ........
8.most safe anti thyroid medication in pregnancy ................
9.RAIU in a) thyroiditis..............................
b) Grave disease ........./
10.hashimoto thyroiditis - HLA .................. // Anti ........... Ab
-Bx
11.viral illness f/b pain in neck (tender thyroid) - .......................
12.fibrosis of thyroid gland ............................. thyroiditis .
13. Excess Iodine leading to hypothyroidism -c/a- .............. ............. effect
14. Delibrate ingestion of thyroxine to loose wait c/a ............. ................

On raising the arm

Goiter
Svc
SVC

RA
RA
Chapter 8
Basics of Adrenal Gland

Medulla

Increase in Aldosteron -

Increase in Cortisol -

Increase in NE/E -

Slow (Gradual) decrease in all adrenal haromones -

Rapid (acute) decrease in all adrenal harmones -


RASS system (Renin - Angiotensin - Aldosteron-System)

Angiotensinogen

ENaC
Gain of ............ & .........

Blood

So loss of ........... & ...........


in urine

ALDOSTERON - leads to S.Na+ .........


S.K+........
S.H+........
Chapter 9
Hyperaldosteronism

Definition Aldosteron so - S.Na + ......... / S.K+............./ S.H+................


From zona ..................................... of adrenal gland.

Etiology

Definition -

1 hyperaldosteronism
2 hyperaldosteronism

Summary
1 hyperaldosteronism 2 hyperaldosteronism
Aldosterone
S.Na+
S.K+
Metabolic
HTN
Renin
Pedel edema
Rx
Chapter 10
Cushing Syndrome

DEFINITION - increase in ........

Pituitary

Cortisol
Level

Cortisol

Time

Etiopathogenesis

Pituitary
Iatrogenic Pituitary tumor Lung cancer
Cortisol
ACTH
Pigmentation
Headache
Hemoptysis

C/f

Blood sugar -
BP -
Work up Cushing suspected

1.Screening test of choice

2. IOC

To differentiate between iatrogenic v/s pitutory tumor / lung cancer

Managment-
1. Cortisol receptor antagonist-

2. Cortisol synthesis inhibitor -

3 .In Cushing Disease to decrease release of ACTH from pituitary


tumor -
Summary of cushing syndrome
1. M/C/C of cushing syndrom -
2. 2nd MCC of Cushing syndrome ............................. ..............c/a .......... ...............
3. earliest pathological change of cushing syndrome -
4. MC C/F -
5. Blood sugar ........................and BP.........................
6. pigmentation of skin is seen if cause of cushing syn is .........................
........................
7. Screening test of choice
8 IOC
9 To differentiate between pituitary adenoma v/s lung cancer -
Chapter 11
Pheochromocytoma

Definition- Tumor of .........................................found in ............

Etiopathogenesis

AORTA

........... % Pheochromocytoma are extra adrenal.


........... % Pheochromocytoma are Malignant .
........... % Pheochromocytoma are bilateral.

C/f - .............. activity of sympathetic system

...rec
....rec

....... metabolism so wt ......


Investigation -
screening test of choice

IOC-

For localization -

Rx

RxOC-

Summary of PCC
A/C/A -
RULE of 10

Rule of 5o -
Rule of 9-

M/C extra-adrenal site


M/C- c/f -

Screening test -
IOC -

RX - ......... blocker f/b .......... blocker .


Chapter 12
Adrenal Insufficiency
1 adrenal insufficiency
Etiopathogenesis

Z.glomerulosa

Z.fasiculata

Z.reticularis

M/C/C- worldwide-
- India
- HIV patients -

C/f - due to decrease in aldosterone - S.Na+......./ S.K+......../S.H+....

-due to decrease in cortisol -


-due to decrease in sex harmone -
-due to increase in ACTH -

IOC -
Rx. -DOC -
- For salt craving-
ACUTE ADRENAL INSUFFICIENCY

Pathogenesis

DOC
Chapter 13
Physiology of parathyroid gland

Secretes

Activation of
Bone

Blood

Blood

Urine

Net effect of PTH - S.Ca+.........../ S.po4 ........../ ALP.............


Chapter 14
Parathyroid Pathology

1 hyperparathyroidism Etiopathogenesis

Definition - increase in PTH due to

Parathyroid gland

Excess ........

Excess activation of ...................

.................................................

Urine
Investigation - PTH........ / S.Ca+........ / S.PO4........ / ALP.......

For localization of tumor -

DOC

RxOC-
2 Hyperparathyroidism

Definition ..............in PTH due to ........

Etiopathogenesis

Absorption of

Parathyroid gland

Blood
Investigation - PTH........ / Vit D........ / S.PO4........ / ALP.......
S.Creatinine........ / S. Ca+2.......

Rx-

Hypoparathyroidism

Etiopathogenesis- .......................... in PTH

Due to .................................

C/f

Chvostek sign. Trosseau sign


ECG
S Ca+2

Rx -

Extra point

Pesudo-hypoparathyroidism Pseudo-Pesudo-hypoparathyroidism

Bone. Kideny Bone. Kideny

Summary
1.effect of PTH ---S.Ca+2 .........and S.PO4..........
2. 1 hyperParathyroidism - MCC -
- Xray skull-
-PTH ........ S.Ca+2 ...... S.PO4.......
3. 2 hyperParathyroidism - MCC -
- Bone defect c/a-
- PTH ........ S.Ca+2 ...... S.PO4.......
4.Hypoparathyroidism - PTH ........ S.Ca+2 ...... S.PO4.......
Carpo -pedal spasm with BP Cuff c/a - ......................... sign.

* Troisier sign---

5.PTH - Both bone and kidney resistant -


- only bone resistant
- associated with .................... gene mutation.
Chapter 15
Basics of pituitary Gland

Hypothalamus Periventricular nucleus


Supraoptic nucleus

Pituitary stalk

Adenohypophysis Neurohypophysis

Prolactin
GH
Antidiuretic harmone (ADH)
TSH
ACTH Oxytocin
FSH/LH

Control of ant. Pituitary

Hypothalamus GHRH Dopamin TRH CRH GnRH

Ant.Pituitary GH Prolactin TSH ACTH FSH/LH


Pituitary injury v/s pituitary stalk injury

Hypothalamus Hypothalamus

Pituitary

Pituitary harmone level - ................ Pituitary harmone level - ................

Prolaction level ........................ Prolaction level ........................

Extra points for pituitary injury

1. Pituitary injury if due to obstetric cuase

2. Pituitary injury if due to obstetric cuase

1 st harmonen to decrease -

Last harmone to decrease -

1st harmone to be replaced via treatment-


Chapter 17
Pituitary disorders

Hyperprolactinemia
Definition - ............................... level of prolactin

Etiopathogenesis-
1. 2. 3
Hypothalamus Hypothalamus

Pituitary Pituitary

Prolactin

C/f- increased prolactin - 1.


2.
3.
screening test -
IOC -

Rx- 1.

2. In pregenancy

3. If compression symptom-

Acromegaly

Definition -

Increase in GH before puberty is called as -

Clinicopathogenesis

Increased GH - ............................ Somatomedins -


Facial feature
Voice
Hand and ring size

Hands looks like .............

GH

1981 1982 1983 1984

Screening test of choice -

Confirmatory test-
For size of tumor

Rx- if resectable tumor -

If non-resectable - initial treatment -


Best drug -

Extra point GH receptor anomaly


Xray foot

SIADH Syndrome of inappropriate secretion of


antidiuretic harmone (ADH)

Etiology - H
E
L
D

Physiology fact
* ADH is secreted from ........ ............ acts on ........receptor
in collecting tubles of nephron and opens .................................
channels which leads to...................................water absorption
from.................
Pathogenesis

SIADH
ADH

V2 receptor

Bloodvolume

Heart
Gain of
.........

Loss of ......... &........

ANP- atrial natriuretic peptide


BNP- brain natriuretic peptide

C/f -

Investigation - IOC -
urine osmolarity ...
Plasma osmolarity ... DOC
Diabetes Insipidus

Post. Post.
Pituitary Pituitary

V2 rep V2 rep

Urine amount Urine amount


Urine osmolarity Urine osmolarity
Plasma osmolarity Plasma osmolarity
ADH level ADH level
IOC
DOC DOC

Extra point
Polyuria ( 3lit./day or >40ml/kg/day)

Urine volume .... Urine volume ....


Urine osmolarity .... Urine osmolarity ....
Plasma osmolarity.. Plasma osmolarity..
Extra point
DM + DI + Optic atrophy -

Endocrine neoplasia
Insulinoma - tumor of ........ cell so .............. insulin

C/f-

Ioc -
For localizing tumor -

Rx-

B-cell hyperplasia is called as-

VIPOMA -
(VIP - vaso active intestinal peptide )

A/c/a -

C/f -
Glucagunoma - tumor of ......cell so ...................

C/f - blood sugar


- skin -

Gastrinoma/ zollinger elison syndome

Tumor or ...... cell. M/c site-


C/f-

Doc-

Multiple endocrine neoplasia (MEN)

MEN 1 MEN 4

overall mc enteropancreatic tumor

M/C pancreatic tumor

MEN 2A MEN 2B (MEN 3)


Summary -

1.Pituitary gland injury - prolactin level .......-


2.Pituitary stalk injury - prolactin level ....
3. Prolactinoma - mcc -
-DOC
-DOC in pregnancy
4.ACROMEGALY - voice
- MC cancer
Screening test
IOC
Xray foot -
Rx- initial
- BEST-
5.SIADH
MCC -
PATHOgenesis -.................................. ....................natremia.
Urine osmolarity - .........
IOC -
DOC

6. Diabetes insipidus
Central - ADH level -
Nephrogenic - ADH level -
Urine osmolarity ...

IOC
rx - central
- nephrogenic -
7. Insulinoma
C/f - ................... triad
IOC -
FOR localization --

8. Glucagunoma - skin finding

9 VIPOMA- c/f - ...........................................


K+. ........ / cl-.........
ARISE - DELHI
Contact :
+ 91 9560022836
+ 91 9560022837
+ 91 9560022838
K261, 2nd Floor Lane No.5,
Westend Marg, Saidulajab,
Saket, New Delhi, Delhi 110030
:arisemedicalacademy.delhi@gmail.com

ARISE - JAIPUR ARISE - HYDERABAD


Contact : Contact :
+ 91 8977541723 + 91 7680929292
+ 91 8977641723 + 91 7396757585
+ 91 9929113115 #: 2nd Floor, Above Indian Bank,
Opp. : Olive Hospital
+ 91 9929113116 Kakatiya Nagar Colony,
Plot No-26, Krishna Vihar, Sector -5, Mehdipatnam, Hyderabad - 500 028
Near Pushp Enclave, Pratapnagar, :arisemedicalacademy@gmail.com
Tonkroad, Sanganer, Jaipur -302033.
:arisemedicalacademyjpr@gmail.com

ARISE - KERALA ARISE - CHENNAI


Contact : Contact :
+ 91 8136932666 + 91 8977941723
+ 91 9633799504 + 91 8977942723
#: 2nd Floor, Kingdom Tower, #: No. A Super 20, Thiru.
Manna, Taliparamba, Vi Ka Industrial Estate,
Kannur, Kerala, India Guindy, Chennai -600032
:arisemedicalacademy.kerala@yahoo.com :arisemedicalacademychennai@gmail.com

You might also like