Plantar Equivalents

Plantar Equivalents complete explanation are give here

General Medicine Lecture Notes - University of California

UC Irvine’s Department of Medicine is a dynamic, multispecialty group of highly engaged physicians and researchers who work at the leading edge of medical discovery and education in order to provide the best and most comprehensive patient care. Residents attend academy lecture. With more than 230 full-time faculty and 160 interns, residents and fellows, the department is the largest within the university’s School of Medicine.

1.    ABGs

2.    Acute Coronary Syndrome

3.    Acute Decompensated Heart Failure

4.    Acute Pancreatitis

5.    Adrenal Insufficiency

6.    A-Fib

7.    AKI

8.    Alcohol Withdrawal

9.    Anemia

10. Antibiotics

11. Blood Transfusion - When to Transfuse and Risks Involved

12. Cellulitis

13. Central Line Infections

14. Community Acquired Pneumonia

15. Constipation in Adults

16. COPD

17. COPD - Gold criteria for classification

18. Cushings Syndrome

19. Decreased Urine Output

20. Delirium

21. DKA

22. ECG for Interns

23. Electrolyte Replacement

24. Foot Ulcers

25. GI Bleeding, Upper

26. GI Prophylaxis, Indications

27. Hospital Acquired Pneumonia

28. Hypercalcemia

29. Hyperkalemia

30. Hypertensive Emergencies

31. Hyponatremia

32. Intern Orientation - Sign Out

33. IV Fluids

34. LFT

35. Lipid Management - 2013 ACC-AHA Guidelines

36. Management of Inpatient Hyperglycemia

37. Mechanical Vent

38. Pain Treatment Options

39. PRBC Transfusions Medicine Floor

40. Proteinuria

41. Opioids

42. Pulmonary Embolism, Diagnosis

43. Renal Stones

44. Sepsis

45. Shock Mini Lecture

46. ST Elevation on EKG

47. SVT

48. Syncope

49. Used PRN Medications

50. Vasopressors and Inotropes

51. Ventilator Basics

52. VTE Prophylaxis

53. Weaning from the Ventilator

What are the named murmurs in cardiology?

Following are the named murmurs.

Still's Murmur

It is the innocent musical murmur ,seen in children.

Austin flint murmur

Mid diastolic murmur heard in apex in patients with aortic regurgitation.

Roger's murmur

It is the loud pansystolic murmur which is heard maximally at the left sternal border.  Heard in Ventricular septal defect (VSD).

Graham Steell murmur

Early diastolic murmur which is heard over Erb's point.Heard in pulmonic insufficiency, secondary to pulmonary hypertension and mitral stenosis.

Carey Coombs murmur

Mid diastolic murmur, heard in acute rheumatic valvulitis.

Rytands murmur 

Occur in complete heart block, this is a mid diastolic  murmur.

Docks murmur

This is a diastolic murmur, occur in left anterior descending (LAD) artery stenosis.

Mill wheel murmur 

Heard  due to air in right ventricular cavity following cardiac catheterization.

Cabot– Locke murmur

Diastolic murmur heard best at the left sternal border. heard in anemic patients .The murmur resolves with treatment of anemia.

Gibsons murmur

Continuous murmur heard in patent ductus arteriosis.Best heard at the left upper sternal border.

Key–Hodgkin Murmur

The Key–Hodgkin murmur is a diastolic murmur of aortic regurgitation .Hodgkin correlated this diastolic murmur with retroversion of the aortic valve leaflets ,seen  in syphilitic aortic regurgitation.

Differential diagnosis of diastolic murmurs of heart

These are Murmurs which occurs during any part of diastole

1.Early diastolic murmurs

They begin with or shortly after second heartsound S2 as soon as corresponding ventricular pressure falls enough below that in the aorta or pulmonary artery

Causes of early diastolic murmurs:

1. AR (aortic regurgitation)-heard in right 2nd ICS (interscapular space) and Erb’s area,increases on expiration
2. PR (pulmonary regurgitation) -left 2nd ICS,increases on inspiration

2.Mid diastolic murmurs

Arise from mitral or tricuspid valves,they occur during  early ventricular filling , produced due to disproportion between valve orifices and flow rate.

Common causes :Mitral stenosis,Tricuspid stenosis

Uncommon causes: 

1. Carey - Coombs’ murmur
2. Austin-Flint’s murmur
3. Acute severe 
4. Ritan’s murmur
5. Flow MDM in high output states

Flow MDM across tricuspid valve occur in 

1. Atrial septal defect
2. Tricuspid regurgitation
3. Total anomalous pulmonary venous connection

Flow MDM across mitral valve is seen in 

1. Ventricular septal defect
2. Patent ductus arteriosis
3. Mitral regurgitation
4. Aortic regurgitation

3.Late diastolic/presystolic murmurs

Begin during period of ventricular filling and follows atrial contraction and therefore occur in sinus rhythm

Causes

1. Mitral stenosis
2. Tricuspid stenosis
3. Atrial myxomas
4. Complete heart block

Heart murmurs (Systolic and Diastolic murmur)

Heart murmurs are relatively prolonged series of auditory vibrations of variable intensity,quality as well as frequency.

Heart murmurs are produced due to turbulence when there is increased blood flow or due to flow through a constricted or irregular orifice.

Description of a murmur

1. Area over precordium where murmur best heard
2. Systolic or diastolic
3. Timing and character
4. Intensity
5. Pitch
6. Bell/diaphragm
7. Conduction
8. Variation with respiration
9. Best heard posture
10. Variation with dynamic auscultation

Levine and freema’s grading of murmur

Systolic murmur

1. Very soft [heard in a quiet room]
2. Soft
3. Moderate
4. Loud with thrill
5. Very loud with thrill [heard with stethoscope]
6. Very loud with thrill [heard even when stethoscope is slightly away from chest wall].

Diastolic murmur

1. Very soft
2. Soft
3. Loud
4. Loud with thrill

Mechanical events of the cardiac cycle

The cardiac cycle
The cardiac events occur from the beginning of one heart beat to the beginning of next heart beat.
It is initiated by spontaneous generation of action potential in SA (sinoatrial ) node.
Duration of one cardiac cycle is O.8 seconds.
Ventricular filling occur during  diastole.


Mechanical events of the  cardiac cycle
1.Atrial systole
2.Atrial diastole
3.Ventricular systole .
Isovolumetric contraction
Rapid ejection
Reduced ejection
4.Ventricular diastole
Proto diastole
Isovolumetric ventricular relaxation
Earlier rapid filling
Reduced filling
Last rapid filling due to atrial systole

Atrial systole
It follows the impulse generation in SA node and atrial depolarisation.
When the atrial muscle contracts, pressure in atria increases.
30% of blood is propelled into ventricle.
Narrowing of opening of SVC and IVC and pulmonary veins occur

Ventricular systole
Isovolumetric  contraction
In isovolumetric  contraction ventricular pressure  exceed  atrial pressure closure of AV valves occur producing first heart sound.
Opening of aortic valve occur when leftventricular pressure is > 8OmmHg.
Opening of pulmonary valve is seen when right ventricular pressure > 10 mmHg.
This will result in small rise in atrial pressure.
Rapid ejection
After opening of the aortic and pulmonary valves, ventricular ejection begins.
Intraventricular pressure rises to a maximum of 120 mmHg in left ventricle and 25mmHg in right ventricle.
2/3rd stroke volume is ejected during this phase.
Reduced ejection phase
Ventricular pressure decreases during this phase.
Arterial pressure increases.

Ventricular diastole
1.Protodiastole 
At the end of ventricular systole, ventricular pressure falls, arterial pressure is more than  pressure inside the ventricle resulting in closure of semilunar valves which produce second heart sound.
2.Isovolumetric ventricular relaxation
Ventricular pressure drop rapidly in this phase ,the ventricular muscle relax without change in ventricular volume.
This phase ends when ventricular pressure drops below atrial pressure resulting in opening of AV valves.
3.Phase of earlier rapid filling
Rapid filling of ventricles occur.
Pressure inside the ventricles remains low.
4.Phase of reduced filling
Filling of ventricles is due to continous venous return filling  both atria and ventricle.
70% ventricular filling.
5.Last rapid filling
Corresponds to atrial systole.
30% filling occur in this phase.

Atrial diastole
Atrial muscle relax and atrial pressure increase gradualy due to continous venous return.
After the opening of atrioventricular valves pressure drops to zero and again slowly rises until the next atrial systole.

What are different Insulin preparations?

Various insulin preparations are available based on onset and duration of action.They can be short acting or long acting.

1. Lispro

Short acting group insulin.

28th lysine & 29th proline in B chain is reversed by recombinant DNA technology.

It has less tendency to form local aggregates.

Lispro has less incidence of hypoglycemia.

Absorption is delayed with NPH insulin, but not with ultralente.

Injected just before or after food.

2. Aspart

This is the shortest acting group of insulin.

This can be protaminated to extend the duration of action.

Aspart + protaminated aspart = Biphasic insulin.

Can be used as 30/70 insulin.

Used in pen devices.

3. Glulisine

Short acting insulin.

Not commonly available.

Asparagine @ B23 position is replaced by Lysine, lysine at B29 replaced by Glutamic acid.

4. Isophane / NPH insulin

Biphasic isophane available as pen devices.(Mixtard 30 novolet).

Most popular in 30/70 combination.

Lente available as Monotard.

Can be used once daily.

Ultara lente not available now.

5. Glargine

Asparagine at 21 replaced by Glycine.

2 Arginine residues added to c terminus of B chain.

Longest acting.

No peak in action,smooth sustained effect.

Less chance of hypoglycemia.

Not stable at room temp.

Cant mix with others.

6. Detemir

Myristic acid is bound to B29 lysine.

Long acting.

No local aggregate is formed.

Bound to albumin.

Less chance of hypoglycemia.

7. Degludec

Newer Long acting.

Effective at physiological pH.

Can be mixed with other insulins.

Treatment of hyperkalemia

Hyperkalemia is a medical emergency.Treatment should be started as early as possible.

Approach to treatment is based on two main factors

1. Degree of hyperkalemia

2. Change in ECG

Aim of treatment 

1.Minimise the membrane depolarization over a few minutes with calcium gluconate

Calcium gluconate

Dose of calcium is 1g of 10% calcium gluconate or calcium chloride which is infused intravenously over 2-3 min; may require repeat dose if no improvement in ECG is seen by 5 minutes.

Onset and duration of action -Immediate onset of action, lasting 30-60 minutes.

Magnitude of [K+] decline-There is no decline in potassium.

Precautions - Calcium chloride should be administered preferably via a central vein to reduce the risk of extravasation and skin necrosis.

2. Shift the potassium into the cell over the next 30 to 60 minutes

This is achieved with following drugs which will shift the potassium into the cell.

a. Insulin

Dose of insulin-is 10unit to 20units of regular insulin IV (with one ampule of Dextrose 50 intravenous fluid if there is no significant hyperglycemia).

Onset and duration of action Onset of action is within 15 to 30 minutes it will last for 6-8 hour.

Magnitude of [K+] decline is 0.5 to 1.5 mEq/L.

Precaution - Watch for hypoglycemia or hyperglycemia (as dextrose is  given),they will affect the K+ lowering effect of insulin.

b. Albuterol

Dose is 10-20 mg ,it is given by nebulized inhalation over 15 minutes or can be given as a continuos nebulized treatment over 30 to 60 minutes OR 0.5 mg of albuterol in 100 mL of 5% dextrose infused intravenously over 15 minutes.

Onset and duration of action Onset is at 30 minutes,lasting for3-6 hour.

Magnitude of [K+] decline is .5 -1.5 mEq/L.

Precautions-Increased heart rate and variable effects on blood pressure can occur .

c. NaHCO3

Dose- 2-4 mEq/minute in drip (3 ampules NaHCO3 in sterile water or 5% dextrose infusion is given till the bicarbonate is normalized.

Onset and duration - Onset of action is at 4 hour, lasting > 6 hr.

Magnitude of [K+] decline -0.5-0.75 mEq/L.

NaHCO3 is not effective I there is concurrent inorganic metabolic acidosis;It can result in volume overload and lower ionized calcium.

3.Long term measures to reduce the serum potassium

a. Loop +/− thiazide diuretics

Dose varry widely depending on GFR(glomerular filtration rate).

Onset start at 30-60 minutes, last for 4-6 hour (duration increased  in renal insufficiency).

Magnitude of [K+] decline is variable depending on the diuretic response.

Better to avoid in volume depleted states until euvolemia is restored.

b. Sodium polystyrene sulfonate

Dose is 25-50 g mixed in 100 mL 20% sorbitol per orally OR 50 g in 200 mL 30% sorbitol per rectum.

Onset of action is at 1-2 hour, lasting 4-6 hour.

Magnitude of [K+] decline is 0.5-1 mEq/L.

Use cautiosly in the postoperative patient because of risk of intestinal necrosis.

c. Hemodialysis

Response based on initial potassium value.

Immediate onset of action, lasting until dialysis completion.

Magnitude of [K+] decline - is variable, based on dialysis dose and dialysate [K+].

Rebound increase in potassium value after dialysis can occur.

Regulation of insulin secretion (Chemical,Hormonal and Neural factors)

Insulin was discovered in 1921 by BANTING and BEST.  

It is a peptide hormone composed of 51 amino acid residues.

Insulin has a molecular weight of 5808.

Insulin is synthesized in the beta cells of the pancreas.

The name insulin comes from the Latin word insula for "island" 

Insulin is initially produced as a single polypeptide chain, preproinsulin which contain 110 amino acid residue.

1unit of insulin is secreted per hour under basal conditions.

Regulation of insulin secretion is by Chemical, hormonal and neural factors

Chemical factors

1. Glucose, amino acids (arginine, etc.), fatty acids, and ketone bodies stimulate  the secretion of insulin. 

Hormonal factors

1. Glucagon increase insulin release
2. Somatostatin inhibits the insulin release
3. Growth hormone,Thyroid hormone,cortisol produce  hyperglycemia.

Neural factors

1. Alpha2 stimulation decreases insulin secretion.
2. B2 stimulation increases the insulin level.
3. Cholinergic stimulation increases insulin.

Drug treatment of Graves'disease

The hyperthyroidism of Graves' disease is treated either by 

1.Reducing the synthesis of thyroid hormone using antithyroid drugs or   

2.Reducing the amount of thyroid tissue with radioiodine (Iodine131) treatment or by thyroidectomy

Antithyroid drugs include

Thionamides such as propylthiouracil, carbimazole and the active metabolite of the carbimazole that is methimazole. 

Effects of these drugs are following

1.Inhibit the function of TPO(thyroperoxidase) 

2.Reduce oxidation and organification of iodide. 

3.These drugs also reduce thyroid antibody levels 

4.They enhance rate of remission. 

Drug dosage

The initial dose of carbimazole or methimazole is usually 10–20 mg given every 8 or 12 h, but after euthyroidism is restored once-daily dosing is possible. 

Propylthiouracil is given at a dose of 100–200 mg every 6–8 h, this drug is given in divided doses are usually throughout the course. 

Lower doses of each drug may suffice in areas of low iodine intake as thyrotoxicosis improves.

Ttitration regimen 

In titration regimen the starting dose of antithyroid drugs can be gradually reduced once euthyroidism is achieved.The titration regimen is often preferred beause of the following

1.To minimize the dose of antithyroid drug 

2.It provides an index of treatment response

Block-replace regimen

Alternatively, high doses may be given combined with levothyroxine supplementation .

The advantage of this regimen is this will avoid drug-induced hypothyroidism. 

Monitoring treatment response

Thyroid function tests and clinical manifestations are reviewed every 3–4 weeks after starting drugs and the dose is titrated based on unbound T4 levels in blood. Most patients do not achieve euthyroidism until 6–8 weeks after initiation of treatment. 

TSH levels often remain suppressed for several months and therefore it do not provide a sensitive index of treatment response

The usual daily maintenance doses of antithyroid drugs in the titration regimen are

2.5mg –10 mg of carbimazole or methimazole

50–100 mg of propylthiouracil

Time taken for remission

Maximum remission rates are achieved by 18–24 months for the titration regimen 

6 months for the block-replace regimen. 

Patients with severe hyperthyroidism and large goiters are most likely to relapse once treatment stops, close follow up is required  in all patients for relapse during the first year after treatment and at least annually thereafter.

The common side effects of antithyroid drugs

Rash, urticaria, fever, and arthralgia (seen in 1–5% of patients).These side effect may resolve spontaneously or after substituting an alternative drug. 

Rare but major side effects include

Hepatitis, an SLE-like syndrome; and,the most important agranulocytosis (seen in <1%).

Antithyroid drug should be stopped and not to be restarted if a patient develops major side effects

Written instructions should be provided regarding the symptoms of possible agranulocytosis (sore throat, fever, mouth ulcers) and the patients should be advised to stop treatment and a complete blood count shoud be checked to confirm that agranulocytosis is not present

Betablockers

Propranolol (20–40 mg every 6 h) or longer-acting beta blockers such as atenolol is given  to control adrenergic symptoms, especially in the early stages of disease.

Beta blockers are especially useful in patients with thyrotoxic periodic paralysis

Anticoagulation should be considered in all patients with atrial fibrillation.Digoxin doses need to be increased in the thyrotoxic state

Clinical features of hypokalemia

Prominent effects of hypokalemia is on heart, skeletal, and intestinal muscle cells.

Effect of hypokalemia on the heart

Hypokalemia is a major risk factor for both ventricular and atrial arrhythmias.

It predisposes to digoxin toxicity 

Electrocardiographic changes in hypokalemia are the following.

Broad flat T waves, 

ST depression, 

QT prolongation

These finding are most marked when serum K + is <2.7 mmol/L.

 Effect of hypokalemia on skeletal muscle

Hypokalemia will results in hyperpolarization of skeletal muscle, hence impairing the capacity to depolarize and contract the skeletal muscle which results in weakness and even paralysis . Hypokalemia can causes skeletal myopathy and predisposes to rhabdomyolysis.

Effect on intestinal smooth muscle

The paralytic effects of hypokalemia on smooth muscle of intestine  may result in intestinal ileus.

The functional effects of hypokalemia on the kidney include

Na + -Cl – and HCO 3 - retention

Polyuria 

Phosphaturia 

Hypocitraturia

Activation of renal ammoniagenesis. 

Retention of bicarbonate and change in other acid-base effects of hypokalemia can predispose to metabolic alkalosis.Polyuria is due to both polydipsia and an AVP-resistant renal concentrating

defect.

Hypokalemia can cause structural changes in the kidney which include 

1.Relatively specific vacuolizing injury to proximal renal tubular cells

2.Interstitial nephritis

3.Renal cysts. 

4.Hypokalemia can also predisposes to acute injury to kidney so lead to end-stage renal disease

This is commonly seen in those patients with long-standing hypokalemia due to laxative abuse or eating disorders

Hypokalemia and/or decreased dietary K +intake is implicated in the pathophysiology as well as in the progression of hypertension, heart failure, and stroke.If there is short-term K + restriction in healthy humans and in patients with essential hypertension that will lead to result in Na + -Cl – retention and hypertension. Correction of hypokalemia is required in hypertensive patients treated with diuretics, because correction of hypokalemia helps to control blood pressure.

Signs and Symptoms of Hypokalemia

1. Alkalosis
2. Shallow Respirations 
3. Irritability
4. Confusion and drowsiness
5. Weakness and fatigue
6. Arrhythmias
7. Lethargy
8. Thready Pulse

Pathogenesis of hepatic encephalopathy

Hepatic encephalopathy is a complex neuro psychiatric syndrome that is caused by liver disease. 

This will manifests as disturbances in

1.Consciousness and behaviour.

2.Personality changes.

3.Asterixis.

4.Distinctive electroencephalographic changes

It may present as 

Acute and reversible form

Chronic and progressive form

Severe cases  may leads to coma, later on death 

Occur in severe hepatocellular dysfunction.

Main  mechanism of hepatic encephalopathy is porto systemic shunting of blood.

This is a complication of portal HTN.

There is obstruction to the passage of blood  absorbed from the intestine to go through liver. As there is no valves in the portal venous system it will facilitates retrograde blood flow to the lower pressure systemic venous circulation. So the portal blood bypass the liver and it reaches the systemic circulation without undergoing the 1st pass detoxification. There is portal systemic collateral formation.The major sites of collateral are Gastro oesophageal junction, umbilicus, anal canal and posterior abdominal wall.

Toxic substances accumulated in hepatic encephalopathy are

False neurotransmitters

Octopamine 

Ammonia 

Mercaptans(methionine metabolism)

Short chain fatty acids

GABA(Gama-aminobutyricacid) inhibitory neurotransmitter

Endogenous benzodiazepine acting through GABA receptors 

What these neurotransmitters will do?

1. These neurotransmitters will causes the supporting cells of the brain (astrocytes) to swell. Which inturn increases the intracranial pressure, leading  to herniation of brainstem and death

2. There will be disruption of the blood brain barrier leading to cerebral edema. 

What are the causes of thyrotoxicosis ?

Thyrotoxicosis is defined as the state of thyroid hormone excess. 

But it is not synonymous with hyperthyroidism, which is the result of excessive thyroid function.

Following are the causes of thyrotoxicosis

• Primary hyperthyroidism 
• Thyrotoxicosis without hyperthyroidism
• Secondary hyperthyroidism 

1. Primary hyperthyroidism

Graves' disease.

Toxic multinodular goiter.

Toxic adenoma.

Functioning thyroid carcinoma metastases.

Activating mutation of the TSH receptor.

Activating mutation of Gs alpha (McCune-Albright syndrome.  Struma ovarii ).

Drugs-iodine excess.

2.Thyrotoxicosis without hyperthyroidism

Subacute thyroiditis. 

Silent thyroiditis.

Other causes of thyroid destruction are amiodarone, radiation, infarction of adenoma.

Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue.

3.Secondary hyperthyroidism

TSH-secreting pituitary adenoma. 

Thyroid hormone resistance syndrome. 

Chorionic gonadotropin-secreting tumors.

Gestational thyrotoxicosis. 

Factors precipitating hepatic encephalopathy

Patients with chronic liver disease are prone to hepatic encephalopathy which manifest as altered sensorium. It may be precipitated by a variety of causes which can be prevented.

1. Increased nitrogen load

Increased nitrogen load is seen in the following conditions

Gastrointestinal bleeding, since the blood contain large quantity of proteins when there is GI bleed, there will be protein load in intestine.It is acted upon by intestinal bacteria leading to  increased NH3

Excess dietary protein intake.

Azotemia

Constipation

2. Electrolytic imbalances

Hypokalemia(secondary to diuretic therapy, paracentesis,vomiting) stimulates renal NH3 production.

Systemic alkalosis.

Hyponatremia

Hypovolemia

3. Drugs

Diuretics produce electrolyte imbalance

Narcotics, sedatives

4. Infections

Superimposed acute viral hepatitis

Alcoholic hepatitis

Extrahepatic bileduct obstruction

5. Surgeries

Atypical manifestations of hypothyroidism

Thyroid hormone can directly influence every cell in the human body.Diagnostic confusion may occur when the functional derangement of one body system dominates the clinical picture.
Following are the common manifestations of hypothyroidism
Weight gain
fatigue
Cold intolerance
Puffy face
Constipation
Pedal edema
Atypical manifestation of hypothyroidism are not so rare.So high index of suspicion is necessary to diagnose the situation, this is very important because the disease is completely reversible and the treatment is cheap.When there is unexplained clinical conditions such as neuropsyhiatric, non responding cardiac,locomotor, gastrointestinal problems and in PUO(pyrexia of unknown origin) rule out thyroid dysfunction (can be hypothyroidism or hyperthyroidism)  including auto immune status.
Psychiatric manifestations of hypothyroidism
Psychiatric symptoms are common in both overt hypothyroidism as well as in subclinical hypothyroidism.Depression may be the first or sometimes the only clinical manifestation in hypothyroidism.Hypothyroidism may manifest as a variety of other neuropsychiatric symptoms which include
Mood disorders
Psychosis
Mania
Bipolar disease
Delusions
Visual and auditory hallucinations
Cognitive dysfunction
Impaired concentration
Decline in intelligence
Memory disturbance
Dementia
Cognitive dysfunction are more pronounced in elderly, hence it should be considered as a reversible cause of dementia.
Dermatological manifestations of hypothyroidism 
Sometimes dermatological manifestations are initial manifestation of hypothyroidism.
This may present as pruritus or urticaria .Symptoms may continue even after correction of hypothyroidism.
Muskuloskeletal manifestations of hypothyroidism
Arthralgia, arthritis
If there Is predominant small joint involvement of hands it mimick rheumatoid arthritis
Hypothyroidism can  also involve large joints producing myxedematous arthropathy is characterized by synovial thickening, ligamentous laxity and  effusion
Hyperuricemia may contribute to joint pathology.
Joint involvement is more common when the hypothyroidism is of autoimmune etiology
Other presentations are 
Infertility
Menorrhagia
Association with other endocrine dysfunction.
Hyponatremia  is seen in 10 % of hypothyroid patients.Mechanism of hyponatremia in hypothyroidism are due to
Reduction in GFR, impairement of water excretion
Inappropriate release of ADH
When there is unexplained reduction in serum sodium, always evaluate thyroid function
Hyperprolactinemia,headache may be a rare manifestation of hypothyroidism.It may be due to increased TRH production,thyrotrope  hyperplasia  and pituitary  enlargement.Normalization of symptoms occur with thyroid replacement.

Clinical features of Iron deficiency anemia

Insidious onset of symptoms with gradual progression is seen.

There will be symptoms of anemia.

Fatigue is the most common complaint.

Other symptoms are irritability, palpitations, breathlessness, dizziness and headache.

Usually people seeks medical attention when Hb is below 7-8 g/dl.

Neuromuscular manifestations of anemia 

Attention deficit, cognitive dysfunction. occasionally - neuralgic pains, numbness and tingling are seen. Rarely raised intrcranialtension & papilledema 

Nail changes in iron defiency

Nails are brittle,fragile and longitudinally ridged.Tytpical thinning ,flattening and koilonychias are seen 

Changes in oral mucosa

1. Atrophy of lingual papillae
2. Filiform (in ant 2/3rd) - first to get atrophied
3. Soreness and burning of tongue
4. Glossitis 
5. Smooth , waxy and glistening tongue
6. Changes reversed after 1-2 wks of iron therapy
7. Angular stomatitis which is also seen in riboflavin & B6 deficiency
8. Dysphagia called as sideropenic dysphagia (paterson-kelly syndrome or Plummer-vinson syndrome)
9. Stomach there is  gastritis & later atrophy
10. Antibodies to gastric parietal cells are seen in in 1/3rd of cases

PICA - habitual ingestion of unusual substances. Eg - pagophagia - purposeful eating of ice is seen in iron deficiency anemia.

Spleen tip is palpable in 10% cases 

Disturbances in menstruation can occur in females

Skeletal changes are observed in children

In cases of long standing Fe deficiency, Diploic spaces are widened, outer tables are thinned

Rarely - hair-on-end appearance is seen.

What are the clinical manifestations of thyrotoxicosis?

The clinical presentation of thyrotoxicosis  depends on the  

• Severity of thyrotoxicosis 
• The duration of disease
• Individual susceptibility to excess levels of  thyroid hormone 
• Age of patient

Common symptoms of thyrotoxicosis are the following

Weightloss inspite of increased appetite.

Heat intolerance and sweating

Hyperactivity, irritability, dysphoria 

Palpitations

Fatigue and weakness

Diarrhea

Polyuria 

Insomnia and impaired concentration

Oligomenorrhea, loss of libido

Signs of thyrotoxicosis

Tachycardia; atrial fibrillation is commonly seen in the elderly

The high cardiac output produces a  
Bounding pulse

Widened pulse pressure 

Aortic systolic murmur 

Warm, moist skin 

Fine tremor of hands

Goiter- diffusely enlarged thyroid,firm,bruit may be heard over the thyroid

Muscle weakness, proximal myopathy 

Hyperreflexia 

Gynecomastia 

Lid retraction or lidlag due to sympathetic overactivity 

Ophthalmopathy and dermopathy are specific for Graves' disease

Thyroid dermopathy

Seen in <5% of patients with Graves' disease, usually associated with moderate or severe ophthalmopathy.

It is most frequent over the anterior and lateral aspects of the lower leg so called as pretibial myxedema), but the  skin changes can occur at other sites,  particularly after trauma. 

The typical lesion of thyroid dermopathy is a noninflammed, indurated plaque which is deep pink or purple in  color and an orange skin appearance. 

Nodular involvement of skin can occur, and the condition may rarely extend over the whole lower leg and foot, thus  mimicking elephantiasis

Thyroid acropachy 

This is a form of clubbing found in <1% of Graves' disease. It is strongly associated with thyroid dermopathy.

Thyroid ophthalmopathy 

What are the clinical features of hemophilia?

Hemophilia is a coagulation disorder which manifest as increased bleeding due to defective clot formation.In mild disease there is infrequent bleeding that is secondary to trauma.

In severe cases there is haemarthrosis, bleeding into soft tissues, muscles  which can be either spontaneous or secondary to minor trauma.

Earliest  bleeding manifestation are seen when the child begins to crawl or walk.

Some people manifest it as increased bleeding after minor surgical procedures.

Joint bleed or hemarthrosis

Severe forms as recurrent haemarthroses are seen in severe factor deficiency.

Common sites of joint bleed are knee,elbows,ankles, hip and shoulders.

Painful local swelling and erythema can occur due to superficial bleed.

Joint bleed may lead to inactivity decreased joint mobility, neutral fixed position may lead to contractures.

Chronic haemarthroses can lead to synovitis.

Vicious cycle of bleeding lead to deformity.

Muscle hematoma 

Large bleed in to the muscle will lead to Compartment syndrome.The haematomas in distal parts of limbs leading to compression of arteries,veins and nerves.

Dangerous sites of bleeding are Oropharyngeal spaces, CNS, retroperitoneum -  These bleed are very fatal.

Pseudotumour syndrome…retro peritoneal bleeding with mass,calcification and inflammation may mimic tumor

Damage to femoral nerve.

Pseudotumours in long bones of lower limbs can damage femoral nerve due to pressure effect.

Haematuria in the absence of genito-urinary pathology can occur in hemophilia.

Classification of hemophilia based on residual activity of factors

Mild -6-30 %

Moderate - 1-5 %

Severe  < 1 %

Clinical manifestations usually correlate with activity of residual clotting factor.

The diagnostic criteria for pseudotumor cerebri

The term bening intracranial hypertension (pseudotumor cerebri) is used to designates a characteristic syndrome of

1. Headache
2. Papilloedema
3. Minimal or absent focal neurologic signs
4. Normal CSF composition.

All of them occurring in the absence of enlarged ventricles or the presence of intracranial mass on CT or MRI.

As it is a syndrome and not a disease pseudotumor cerebri has a number of causes or pathogenic associations. The most common form of pseudotumor cerebri is benign or idiopathic intracranial hypertension.

The diagnostic criteria include

1. Symptoms and signs that are restricted to those of elevated intracranial pressure. 
2. Normal findings on neuroimaging studies that is CT and MRI
3. Excluding nonspecific findings of raised intracranial pressure 
4. Increased cerebrospinal fluid (CSF)pressure with a normal composition.
5. When the CSF content is abnormal the diagnosis of idiopathic pseudotumor cerebri should not be accepted.

Consequences of raised intracranial pressure

Intra cranial hypertension literally means that the pressure of the CSF which surrounds the brain is too high.Raised intracranial pressure is transmitted along the paths of the optic nerves, thus causing the nerves to swell resulting in papilledema, which can lead to loss of vision and blindness.