Notesale: Turn your study into money

Document Preview

Extracts from the notes are below, to see the PDF you'll receive please use the links above

---

Khaled khalilia
Diabetes mellitus
DM Type I

DM Type 2

Def:





S+S:

Dx:

Immune mediated β-cell destruction  absolute insulin deficiency
Children (X <30)
Associated with HLA-DR3, HLA-DR4








Polyuria (nocturia)
Polydipsia
Polyphagia
Rapid Unexplained weight loss
...
5
Screenings TESTS:
o
BP
o
Foot
o
Annual dilated-eye exams
o
Annual microalbuminuria
o
Lipid profile every 2–5 years
...

Mostly in DM- type 1
Insulin deficiency

















Polydipsia (Thirst)
Polyuria
Polyphagia (↑hunger,↑ appetite)
Abdominal pain
Dehydration, Hypovolemia
Dyspnea
↑HR
Hyperventilation
↑RR ( kussmaul breath)
Aceton Breath
Cerebral edema











Hyperglycemia (x > 250)
Ketosis
Metabolic acidosis
↓PH (6
...
3)
↓Na²
↑Anion gap
Bicarbonate (most accurate measure of severity)
Osmolality (300-320)
Dipstick  Glucose, ketones





Hyperglycemia
Ketosis
Metabolic acidosis





Non - compliance (Insulin)
Dehydration (chronic)
elderly











Et:

complication of diabetes mellitus (predominantly type 2) in which high
blood sugars cause severe dehydration, increases in osmolarity
(relative concentration of solute) and a high risk of complications,
coma and death
DM Type 2

Onset  insidious
Hyperglycemia (600-1200mg/dl)  X >600
Hyperosmolarity (X > 350)
PH > 7
...










Et:








Exogenous insulin
Autoimmune
Insulinoma
↓Cortisol
Alcohol
Glycogen storage disease
Chronic renal failure

Whipple’s triad:
 Glucose < 45 mg/dl
 Neuroglycopenic symptoms
 Glucose administration  relief

Glucose  80-120 mg/dl
HbA1C ≤ 7
LDL < 100
HDL >
TAG (Tri-acyl-glyceride)  <150

 BP  goal X < 130/80
o ACE-I (Lisinopril, captopril) or

S+S:

o ARB ( Valsartan, Losartan)






Glucose < 45 mg/dl
Neuroglycopenic symptoms (dizziness, headache, fatigue, cloudy vision)
Rapid relief after Glucose administration
Palpitation, sweating, anxiety, tremor, tachycardia





Electrolytes, Glucose-level, cortisol
Insulinoma ?!
C-Peptide  to distinguish between Exogenous Vs
...

Associated with an ↑ risk of CAD and cardiovascular mortality

S+S  Criteria:

Abdominal obesity (↑ waist) X > 40 inches (M) and x > 35 (F)

Triglycerides ≥ 150 mg/dL
Waist > 40 (35)

HDL X < 40 mg/dL (M) and X< 50 (F)
TAG ≥ 150

BP ≥ 130/85
HDL < 40 (50)

Fasting glucose ≥ 100 mg/dL
BP ≥ 130/85
Tx:
FBG ≥ 100

Weight loss

Cholesterol lowering

BP control

Metformin  slow the onset
of diabetes

Screening:
Every year:

dilated eye examination

lipid profile

medical nutrition therapy and education

diabetic nephropathy  dipstick assessment of urine protein

foot examination (by physician)
every 3 months:

HgA1c

BP
Every day:

Home glucose measurements

Foot examination by patient

Khaled khalilia

3

Khaled khalilia
Pituitary and Hypothalamic Disorders
Cushing’s syndrome

Hyperaldosteronism

Def: chronic glucocorticoid excess (Endogenous, Exogenous)

Def:

Et:



















Moon Face
Buffalo hump
Deposition of adipose tissue
...

Long-term corticosteroids use (exogenous)
Adrenal Hyperplasia





Surgery:
Pituitary source  Remove Transsphenoidal
Adrenal source  remove  laparoscopy

Et:

S+S:

overproduction of Aldosterone despite ↑BP and ↓Renin
Primary: production stimulus within adrenal gland
...
(X > 30 = aldosterone hypersecretion)
CT  only after chemical testing:
o
↓K
o
↓Renin
o
↑Aldosteron

Dx:


Dx:






Unilateral adrenal adenoma (70%)
Bilateral Hyperplasia

Tx:

Tx:

24h-urine cortisol  cushing syndrome dexamethsone suppression test (high dose):

Suppressed  pituitary adenoma  do MRI

Not suppressed  not pituitary  ACTH-level (cause):
o
↑ACTH  adrenal Hyperplasia (ectopic), lung  do CT (chest)
o
↓ACTH  Adrenal neoplasia

Khaled khalilia




Adrenal adenoma (unilateral0  surgical resection
Bilateral Hyperplasia  Spironolactone (block aldosterone)

4

Khaled khalilia

Adrenal Gland

Diabetic ketoacidosis

DDK Vs
...
Diabetes insipidus

Serum
Na

Serum
Osmo

Urine
Osmo

SIADH

↓

↓

↑

Dyehydration

↑

↑

↑

Diabetes insipidus

↑

↑

↓

Disorder

Khaled khalilia

5

Khaled khalilia

Adrenal insufficiency

Pheochromocytoma

Def:

Def:




Primary:  adrenocorticoid insufficiency (Addison Disease)
Secondary:  Caused by ↓ ACTH production by the pituitary
slow progressive disease




Et:

Et:









Autoimmune
Idiopathic atrophy
Infection (TB, CMV, Fungal)
Trauma
Hemorrhage, thrombosis, embolism  destroys gland
Drugs: ketoconazole (inhibit cortisol)
Metastatic cancer to the adrenal gland
Sudden removal of chronic steroids (prednisone)






Fatigue, irritability, weakness
Hyperpigmentation (only in primary)
Nausea, vomiting, anorexia, weight loss
Hypotension (↓BP)











↓Na
↑K
Hypoglycemia
Metabolic acidosis
↑ BUN
Eosinophilia **
Cosyntropin stimulation test (synthetic ACTH) (most specific) 
measure the cortisol level before and after administration
...

Nonmalignant







Associated with:
MEN IIa, MEN IIB
Von- Hippel- lindau
Paraganglioma
Neurofibromatosis








↑ BP (Hypertension)
Headache
Sweating
Palpitation
Tachycardia
Tremor







Free metanephrin in plasma (best initial)
24-hour urine metanephrin (confirmation, most sensitive)
Direct measurement of Epinephrine & norepinephrine
CT (adrenal gland)  only after biochemical testing
MIBG scan  nuclear isotope scan






α-Blocker  phenoxybenzamine (best initial)
Ca²-channel blocker, β-Blocker
Surgery  resection
Preoperatively, use α-adrenergic blockade first (1-4 weeks before) to
control hypertension, followed by β-blockade to control tachycardia
...


Dopamine agonist  Cabergoline (better tolerated than
Bromocriptine)
...

Central DI : Insufficient ADH due to:
o
Stroke
o
Tumor
o
Trauma
o
Hypoxia
o
sarcoidosis, infection
Nephrogenic DI : (renal resistant to ADH action)
o
Chronic pyelonephritis
o
Amyloidosis
o
Myeloma
o
Sickle cell disease
o
Hypercalcemia ↑Ca²+
o
Hypokalemia ↓ K
o
Lithium

Treat underlying cause
Fluid restriction
Vasopressin receptor antagonist (Tolvaptan)
Demeclocycline






Rule out psychogenic polydipsia and osmotic diuresis
↑ Na²+ (Hypernatremia)  oral replacement insufficient
↓Urine Osmolality, ↓Urine Na²+ , Serum Osmolality ↑
To differentiate between Central and Nephrogenic it is determined
by the Response to Vasopressin (Desmopressin): DDAVP
Central :
o
↓urine volume
o
↑ Urine osmolality
Nephrogenic:
o
No effect of Vasopressin

Tx:
Central DI  Vasopressin (Desmopressin)
Nephrogenic DI 
o
Correct underlying cause (Hypokalemia, Hypercalcemia)
o
Hdrochlorothiazides

Khaled khalilia

Serum
Osmo

Urine
Osmo

↓

↓

↑

↑

↑

↑

Diabetes insipidus

Dx:

Serum
Na

Dyehydration

Large volume of diluted urine (Polyuria)
Polydipsia (excessive thirst)
Dehydration
Hypernatremia (Na²+)
Confusion, disorientation, lethargy









Tx:

SIADH









↓Na (Hyponatremia X<130)  Na-excertion
↓Plasma Osmolality (X < 270)  ↑water retention
↑Urine Na (X>40)  Na-excertion

Dx:

S+S:



Stress (pain, nausea, postsurgical)
Malignancy (lungs, pancreas)
CNS (inflammation, Guillain-barre-syndrome)
Respiratory (TB, pneumonia)
Drugs (SSRI, cyclophosphamise, nicotine, morphine)

↑

↑

↓

Disorder

8

Khaled khalilia
Thyroid diseases
Hyperthyroidism ↑
Def:





Hypothyroidism ↓
Def:

Elevation of thyroid hormones  T3, T4
Primary  ↑T3/T4 (thyroid)  ↓TSH
Secondary  ↑TSH (pituitary)  ↑ T3/T4













o
o
o
o
o
S+S:

Graves’ disease
Toxic multinodular goiter
Toxic adenomas
Subacute thyroiditis
Exogenous intake

Goiter
Constipation
Weight gain↑
Fatigue, lethargy, coma
Cold intolerance
Bradycardia (↓HR)
↓Reflexes
Hypothermia ↓
↓ Appetite
Hair loss
Edema
Galactorrhea

Et:




















Tachycardia (↑HR)
Palpitations
Arrhythmia (atrial fibrillation)
Diarrhea
Weight loss
Anxiety, nervousness, restlessness
↑ Hyperreflexia
Heat intolerance
Fever
Goiter
Warm, moist skin
Grave’s disease  Exophthalmos, pretibial myxedema, thyroid bruits
Hypercalcemia  because of activated osteoclasts
Insomnia
sweating
Acropathy
Dermopathy
Opthalmopathy




TSH –Level
T4, T3 (mainly T4)







radioactive 131 Iodine thyroid ablation
Propylthiouracil (PTU)
Methimazole (MMI)
β-Blocker  propranolol (for symptoms)
Levothyroxine  to prevent hypothyroidism in patients who have
undergone ablation or surgery
...

Most common cause of thyrotoxicosis
↑ Female
Familial predisposition
HLA B8, DR3



Dx:











TSH level ↑
T3, T4 ↓ (mainly T4)
Serology: Anti-TBO, Anti-Tg
Biopsy  most accurate



levothyroxin

S+S:
Autoimmune (defect in T-suppressor cells)
Immune response after iodine excess, lithium therapy, infection,
postpartum
...


Myxedema coma (crisis)

Tx:







Thionamides:
o
Propylthiouracil (PTU) or
o
Methimazole (MMI) (contra: pregnancy)
o
Inhibit thyroid hormone synthesis (- peroxidase)
o
Inhibit T4  T3
o
Side effects: Agranulocytosis, hepatitis, arthralgia, fever
β-Blocker  propranolol (for symptoms)
Thyroid ablation (radioactive Iodine)  contraindicated: pregnancy
Thyroidectomy (Total/Subtotal)
Stop smoking  

Def:


lifethreatining complication of severe, untreated Hypothyroidism,
percipitated by: infection, Cold, medication
...












Nodule / Nodules
Similar to Grave’s disease, but in Grave no nodules
Tachycardia
HF
Arrhythmia (Atrial fibrillation)
Weight loss
Nervousness
↓ TSH
Weakness
↑ T3, T4
Tremor
↑ Uptake in nodules






TSH  best initial
RAIU  Radioactive iodine uptake  Most accurate
Normal TSH – level + Nodule  could be Cancer **
No need for Biopsy or FNA  because carcinomas are non-functional
...

↑ T3, T4
↓ TSH
↓ Uptake
TSH-Level (best initial)
Depends on what are you suspecting:
If u suspect Grave’s disease  Serology for TSI
If u suspect Thyroiditis  RAIU Scan (Damaged Gland  ↓Uptake)




Pain  NSAIDS, Prednisone
Β-Blocker  treat symptoms

S+S:

Dx:

Tx:

S+S:

Dx:

Tx:

Factious (exogenous) Hyperthyroidism
Def:

Khaled khalilia

Khaled khalilia
Thyroid disorders
Thyroid Storm (thyrotoxic crisis)
Def:



Notes




Precipitated by infection, trauma, surgery









Et:

Acute exacerbation of all of the symptoms of Thyrotoxicosis presenting
in a life threatening state secondary to uncontrolled Hyperthyroidism
...
Solid
 Radioisotope thyroid scan:
o Test for structure
o Differentiate between Hot and cold nodule
...

 Cold Nodule  non-functioning  ↑ malignancy  do
US, FNAB
 RAIU (Radioactive iodine uptake):
o Test of function  order if patient is thyrotoxic
o Measures the turnover of iodine by thyroid gland
o ↑ Uptake  Gland is overactive (Hyperthyroid)
o ↓Uptake 
o
Gland is leaking thyroid hormones (Throiditis)
o
Exogenous thyroid hormones
o
Excess iodine intake (amiodarone, contrast dye)

Khaled khalilia

13

Khaled khalilia

Multiple Endocrine Neoplasm



MEN-1:






Neoplastic syndromes involving multiple Endocrine Glands
Neuroectodermal origin
Autosomal Dominant
MEN 1 (3PPP)
 Pituitary
 Parathyroid
Pituitary adenoma (Ant)  prolactinoma
 Pancreas
o
Headache
o
Visual field defects
o
Galactorrhea
o
Amenorrhea
o
Acromegaly
o
↓Lipido
Parathyroid: (primary Hyperparathyroidism)  Hyperplasia
o
Hypercalcemia
o
Nephrolithiasis
o
Bone abnormalities
Pancreas: (Gastrinoma, inulinoma, vipoma, carcioid syndrome,
Pancreatic tumor)
o
Anemia
o
Anorexia
o
Rash
o
Diarrhea

MEN – 2A:

Medullary Thyroid Cancer (MTC):
o
Neck mass
o
Thyroid nodule
o
Lymphnodes

Pheochromocytoma:
o
Hypertension (BP↑)
o
Palpitation
o
Headache
o
Sweating

Parathyroid (Hyperparathyroidism):
o
Hypercalcemia
o
Nephrolithiasis
o
Bone abnormalities
MEN - 2B:






Notes

Medullary Thyroid Cancer (MTC):
o
Neck mass
o
Thyroid nodule
o
Lymphnodes
Pheochromocytoma:
o
Hypertension (BP↑)
o
Palpitation
o
Headache
o
Sweating
Mucosal + GIT-Neuroma:

MEN 2-A
 MTC
 Pheochromocytoma
 Parathyroid

MEN 2 -B
 MTC
 Pheochromocytoma
 Mucosal + GIT Neuroma

Khaled khalilia

14

Khaled khalilia
Metabolic Bone disease
Osteoporosis
Def:





Et:




S+S:

Osteomalacia/Ricketes

Characterized by ↓ Bone mass and microarchitectural deterioration of
Bone tissue  ↑increase in Bone fragility and susceptibility to fracture
...
5
Osteopenia: T-score between (-1) --- (-2
...
)
X-ray  fractures (best first step if there are signs of fracture)
CBC: pancytopenia  multiple myeloma
TSH  Hyperthyroidism





Bisphosphonate: (Alendronate, Risedronate,)
Smoking cessation and weight-bearing exercises
Estrogen replacement therapy

Khaled khalilia

15

Khaled khalilia

Hypercalcemia ↑
Def:



Hypocalcemia ↓
Def:

Elevated serum Ca2+ > 10
...
4 mg/dl





Et:













S+S:

Primary Hyperparathyroidism (most common)
Drugs: (diuretics (thiazides), PPI, Lithium, Tamoxifen)
MEN-1
MEN-2a
Pheochromocytoma
Immobilization
Paget’s disease
Thyrotoxicosis
Malignancy ( Lung, renal, breast, ovarian )
Hodgkin’s disease
Sarcoidosis
↑ Vitamine D intake
↑ Vitamine A




BONES, STONES, GROANS, PSYCHIC OVERTONES
Cardiovascular:
o
Arrhythmia
o
Shoooooooort QT
o
Ca2 depositions (Valve)
GIT:
o
Constipation
o
Nausea/vomiting
o
Pancreatitis
o
PUD
Renal:
o
Diabetes insipidus (nephrogenic)
o
Nephrolithiasis (stones)
o
Renal failure
Rheumatology:
o
Gout, Pseudogout
o
Boner pain
o
Osteoporosis
Neurological:
o
↓Reflex, ↓Tonus
o
Psychosis
o
Anxiety, Depression









Tx:

Total Corrected serum Ca2+ < 8
...
8 Ca decrease)
...
7) hyperexcitability
(tetany) seen in hypocalcemia
...


Dx:

Tx:

Saline (at ↑Volume)
Bisphosphonate (1st choice)  (Pamidronate, Zoledronic acid)
Corticosteroids (prednisone)  used in Sarcoidosis, malignancy
Dialysis  in Renal failure

Paget’s Disease
Def: Metabolic disease characterized by excessive bone destruction and repair
...

Peptic Ulcer (Ca stimulate Gastrin)
Nephrolithiasis, renal failure, Osteoporosis
...

↑Familial
Hyperparathyroidism

Symptomatic  pain medicaments
Vitamin D, Ca
If ALP > 3x normal  Bisphosphonates

S+S:

Dx:

Tx:

Tx: Surgery (Resection)  when not possible  give Cinacalcet

Khaled khalilia

16

Khaled khalilia

17

Reproductive System
Hypogonadism
Primary Hypogonadism (Hyper gonadotropic Hypogonadism)
Def:

Primary Testicular Failure

↑LH

↑FSH

↓ Testosterone, Sperm count
Et:

Congenital:
o
Klinefelter syndrome
o
Noonan Syndrome
o
Cryptorchidism
o
Bilateral anorchia (vanishing testicle syndrome)

Infection:
o
TB
o
Mumps

Physiological:
o
Trauma
o
Testicular torsion
o
Varicocele

Drugs:
o
Spironolactone
o
Ketoconazole
o
Glucocorticoid
Secondary Hypogonadism (Hypogonadotropic Hypogonadism):
Def:

Hypothalamic-pituitary axis failure

↓LH

↓FSH

↓ Testosteron, Sperm count
Et:

Congenital:
o
Kallman’s syndrome
o
Prader-willi syndrome

Infection:
o
TB

Endocrine:
o
Cushing’s syndrome
o
Hyper/Hypothyroidism
o
Hypothalamic-pituitar disease (Tumor, Hyperprolactinemia)

Chronic diseases:
o
Cirrhosis
o
Sarcoidosis
o
Hemochromatosis
Dx:

Testicular Size / consistency (Soft/Firm)

Sperm count

FSH, LH ,testosterone

Karyotype (primary)

Prolactin level (secondary)
Tx:

Testosterone (improve lipido, muscle mass, hair growth, bone mass)

GnRH-agonist  restore fertility


Hyperandrogenism
Def:









Premature adrenarche
Drugs: (steroids, ACTH, androgens)
PCOS
Congenital adrenal Hyperplasia
Tumors (adenoma, carcinoma)
Cushing’s disease
Hyperprolactinoma



Et:

State of having excessive secretion of androgens (DHEA, Testosterone)
...


Dx:



Tx:

Khaled khalilia

Testosterone, DHEA-S (measure of adrenal androgen production)
LH/FSH
CT/MRI





Stop drugs
Oral contraceptives
Surgery (resection of tumor)

Khaled khalilia

Khaled khalilia

18

Khaled khalilia
2+

Ca - Hemostasis

Khaled khalilia

19

Khaled khalilia

Khaled khalilia

20

Khaled khalilia

Khaled khalilia

21

Khaled khalilia

Khaled khalilia

22

Khaled khalilia

Khaled khalilia

23

Khaled khalilia

Khaled khalilia

24

Khaled khalilia

Khaled khalilia

25

Khaled khalilia

Khaled khalilia

26



---