RESPIRATORY SYSTEM

BRONCHIAL ASTHMA:
Bronchial asthma is a chronic inflammatory disorder which is characterized by bronchial
hyper responsiveness of the airways to various stimulant, leading to wides spread Broncho
construction, air flow limitation and inflammation of bronchi causing symptoms of cough,
wheeze, chest tightness and dyspnoea.
SYMPTOMS: -
 Shortness of breath (or) dyspnoea.
 Chest tightness (or) pain.
 Wheezing.
 Coughing (or) wheezing attacks.
 Trouble sleeping.
ETIOLOGY: -
1. Tobacco, smoke.
2. Infection such as cold, pneumonia.
3. Allergens such as pollen, dust.
4. Drugs such as NSAID, Aspirin and β. blocker.

PATHO PHYSIOLOGY: -
(Reversible condition)
Trigger factors
↓
Release of inflammatory mediators
↓
Activator of inflammatory cells (eosinophils).
↓
Airway inflammation
↓
Hyper secretion. Air muscle contraction of mucus
↓
Narrowing breathing passage
↓
Wheezing, cough, dyspnoea, chest tightness.
DIAGNOSIS: -
 Lung function test
 spirometry.
 peak expiratory flow rate. (PEFR)

TREATMENT: -
 Leukotriene antagonist
montelukast,zafirlukast.
 Bronchodilators
methyl xanthines theophylline, aminophylline
 Anticholinergic
Ipratropium bromide,triolropium bromide

Sympathomimetic -selective β2 agonist.

 Short acting B activity
salbutamol,terbutaline.
 Long acting beta activity
salmeterol,formeterol.
 Must cell stabilizers
sodium cromoglycate.
 Corticosteroids
Beclomethasone, Budesonide,fluticasone, propionate.

NON PHARMACOLOGICAL TREATMENT: -

 Patient and family education to understand to their disease and to fortune self-
confidence and fitness.
 Avoid smoking
 Reduce exposure to indoor allergens.
 To breathing exercise like pranayama
 To physical exercise
 Avoid beta blockers, aspirin,nsaid's.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

COPD is the group of lung disease that makes it hard to breathe and worsen with time.
TYPES:
COPD can be classified into two major type:
1. EMPHYSEMA:
It affects the air sac in the lungs as well as walls between them they become damaged and
less elastic.
2. CHRONIC BRONCHITIS:
In which lining of airways it's constantly irritated and inflamed this cause the lining to swell
and make mucous.
CLINICAL FEATURES:
STEP 1: SYMPTOMS ARE MILD INCLUDE
 Persistent cough dry or with mucous
 SHORTNESS of breath an exertion
STEP 2: MODERATE
 Persistent cough with mucus that worse in morning
 Shortness of breath with mild routine activity
 Wheezing disturbed sleep
STEP 3: SEVERE
 Frequent respiratory tract infection
 Chest tightness
 Swelling in mucosa lining
 Wheezing when doing regular task
STEP 4: FINAL STAGE
 Barred shaped chest
 Constant wheezing
 Heart rate
 ↑BP less of appetite

ETIOLOGY
 Cigarette smoking account 85-90%
 Occupational exposure to chest chemical
 Alpha, anti-trypsin deficiency
 Chronic iv use of cocaine methadone and heroine
PATHOPHYSLOLOGY
Genetic susceptibility
(α1 AT deficiency)
↓

↑ in lungs ability to prevent damage to lung tissue → 1

↓
Free radical produced in lung → 2
Factors like smoking, pollution
In activation of lung proteases → 3

From 1,2,3
↓
Lung inflammation ↑sed oxidation stress inflammatory cytokines and protease
function

Continued repeated injury of bronchial tree ↑sed protolytic destruction of lung

Parenchyma
↓ ↓
Chronic bronchitis Emphysema

TREATMENT:-

Pharmacological treatment
 Bronchodilators
β2aganist →SABA -salbutamol
LABA - salmeterol, formeterol.
 Anticholinergic
ipratropium bromide(short acting)
tritropium bromide (long acting)

 Corticosteroid → oral/IV/inhation
budesomide fluticasone

NON PHARMACOLOGY:-
 Surgery –bullectomy (removal of bullae)
 Lung volume reduction surgery
 Transplant
 Life style change
 smoking
 avoid exposure to dust and chemical fumes
 Long term oxygen therapy.
ENDOCRINE SYSTEM
DIABETES: -
Diabetes Mellitus is the Metabolic disorder Characterised by hyperglycaemia and is due to
deficiency of Insulin.
TYPES:
They are type of diabetes mellitus:
 Type I DM →Insulin dependent DM (IDDM)
 TYPE II DM→Non - Insulin dependent DM (NIDDM)

1. IDDM or juvenile onset DM

↓
Lack of Insulin Secretion Start at child
2. NIDDM or Maturity onset DM (adequate insulin secretion)
↓
At aged people
TYPE -1
 It results from pancreas failure to produce enough insulin
TYPE -2
 It begins with insulin resistance a Condition in which cells fails to response a insulin
properly
SYMPTOMS:
 Increased hunger - Polyphagia
 Increasedthirst -Polydipsia
 Urine Output -Polyuria
 Weight loss- (In Type 1 Type 2)
 Blurred Vision
 Tiredness
RISK FACTOR :( TYPE 2)
 Obesity
 Age 45 years
 Family history
 Physically inactive
 HT, High Cholesterol
RISK FACTOR :(TYPE 2)
 Genetic
 Infection

COMPLICATION:
 Neuropathy
 Nephropathy
 Retinopathy & Vision Loss
 Hearing loss
 Delay wound healing
 Dementia (Memory loss)

PATHOPHYSIOLOGY: -

Type-IDM

Genetic and environmental factor (Viral Infection)

↓
Activation of immune cells
↓
Auto immune Response
↓
β- cells destruction
(Islets of Langerhans damage)
↓
β-cells deficiency
(deceased or no production of Insulin)
↓
DM
 TYPE-II DM

GENETIC FACTOR
↓
Insulin resistance (produce insulin but not utilize it)
↓
βeta-cells dysregulation
↓
Inspired glucose tolerance
↓
βeta-cells in sufficiently
↓
Diabetes Mellitus
DIAGNOSIS:
 Fasting blood sugar
 post prandial blood sugar
 Hemoglobin A1C(HbA1C)
 Lipid profile
TREATMENT:
TYPE- II
 Sulfonyl urea
Glibenclamide
Glimipride
Glipizide
Glidazide
 Biguanides
Metformin
 Thiazolidinedions
Pioglitazone
 Alpha - glucosidase inhibitors
 Acarbose,voglibose,Miglitose
TYPE-I

INSULIN ANALOGUES:
 Short acting - Regular insulin
 Intermediate acting - isophane/NPH
 ultra-short acting / Radid acting - Aspart
 Long acting - Glasgine, determine

NON PHARMACOLOGY:
 Maintain normal body weight
 Reduce intake of carbohydrate rich foods
 Physical exercise (insulin sensitivity)
 Avoid smoking, stress, alcohol
 Monitor blood glucose level regularly
 Adopt personal hygiene to avoid infection
THYROID DISORDER:
Thyroid gland is very essential for growth and development, regulation of energy
metabolism and body temperature.
HORMONES: -
 Triiodothyronine (T3)
 Thyroxine (T4)
 Calcitonin
Synthesis: -
DEFINITION: -
Thyroid disease causes thyroid gland to make either too much of to little of thyroid
hormones.
TYPES: -
 HYPERTHYROIDISM: -
when thyroid gland makes more thyroid hormones than our body needs
 HYPOTHYROIDISM: -
When thyroid gland doesn't make enough thyroid hormones.
SYMPTOMES: -
HYPERTHYROIDISM: -
 Weight loss
 Increase appetite
 Heat in tolerance
 Hair nail growth
 Sweating
 Tachycardia
 Anxiety
 Nervousness, Diarrhoea
HYPOTHYROIDISM: -
 Weight gain
 Loss of appetite,
 Cold intolerance
 Hair loss, Thin nail
 Dry skin
 Brady cardia
 Fatigue,
 Depression, constipation.
CAUSES /ETIOLOGY:-

HYPERTHYROIDISM: -
 Graves disease (Goitor)
 Nodules
 Excessive iodine.

HYPOTHYROIDISM: -
 Thyroiditis
 Hashimoto's thyroiditis, post partum thyroiditis,
 Iodine deficiency.

PATHOPHYSIOLOGY:-
Thyroid dysfunction

Graves disease, → Hashimotor disease

multinodular , → Pituitary failure
↓ ↓
Overactive of thyroid gland underactive of thyroid gland
↓ ↓
↓TSH,T3 and T4 ↑TSH,T3 and T4
↓ ↓
Hyperthyroidism Hypothyroidism

DIAGNOSIS:-
 Thyroid function test.
TREATMENT:-
HYPERTHYROIDISM:-
PHARMCOLOGICAL TREATMENT

 Thioureas
Propylthiouracil, methimazole, carbimazole.
 Iodide
Potassium iodide
 Radioactive iodine
sodium iodide (131I)
NON PHARMACOLOGICAL TREATMENT:-
 Thyroid Ectomy(surgical removal of thyroid gland )
 High calorine diet to replace all energy.
 Drink plenty of water and juice.
 Avoid iodine rich food.
HYPOTHYROIDISM: -
PHARMACOLOYICAL TREATMENT :-
Levothyroxine(L—Thyroxine).
Liothyronine

NON PHARMACOLOGICAL TREATMENT :-

 Avoid eating fatty foods.
 Take iodine rich diet. egg, dairy product, meat and sea food, iodized
salt.
 High fiber food - whole grains (cereals, Barley, Brown rice).
 CENTRAL NERVOUS SYSTEM

EPILEPSY
  Epilepsy is a common neurological condition characterised by recurrent seizure,
loss of consciousness with or without body movement. It is also known as
seizure disorder.
 Seizure is characterised by excessive hyper synchronous discharge of cortical
neuronal activity.
TYPE:
PARTIAL SEIZURE: (FOCAL SEIZURE)
a) simple partial seizure
b) complex partial seizure
GENERALISED SEIZUR:
a) Absence seizure
b) myoclonic seizure
c) Colonic seizure
d) Tonic seizure
e) Generalised tonic - colonic seizure (grand - mal epilepsy)
f) Atonic seizure
CAUSES:
1. Inherited/ genetic
2. Head trauma, neuro surgery
3. Metabolic disorder ( hypoglycemia ,hypercalcemia)
4. Congential malformation
5. WITHDRAWAL OF DRUG:
Alcohol, benzodiazepine, barbiturate
6. DRUGS: some anaesthetic, antibiotic, antipsychotic etc...

RISK FACTOR:
1. Sleep deprivation
2. Alcohol withdrawal, recreational drug
3. Flickering light (include tv, computer misuse screens etc...)
4. Un common reasons like: Loud noises, very hot baths etc.

SYMPTOMS:
  temporary confusions
 staring spell
 uncontrollable jerking movement of arms and legs
 lots of consciousness/weakness
 anxiety, fear
PATHOPHYSIOLOGY:
Excitatory neurotransmitter Na+ ,Ca+, influx
Aspartate, Glutamate↑
Imbalance epilepsy
Inhibitory neurotransmitter
Cl - out flux ↓

Imbalance between inhibitory and excitatory transmitter

↓
Abnormality in ion channels
↓
Abnormal firing /repetitive hypersynchronous neuronal discharge
↓
Epilepsy

TREATMENT: -
 Barbiturates
Phenobarbitone
 Benzodiazepines
clonazepam, diazepam, lorazepam,
 Cyclic GABA analogues
Gabapentin,pregabalin
 Newer agent
Levetiracetam, topiramate, zonisamide.

DIAGNOSIS: -
  ECG (electro encephalogram
 CT scan, MRI scan
 PET (Positron Emission Tomography)

NON – PHARMACOLOGICAL MANAGEMENT: -

 Take ketogenic diet (high fat moderate) proteins, low carbohydrate
 Vagal nerve stimulation
 Avoid stress, sleep deprivation, intake of caffeine, alcohol

ALTERNATIVE THERAPHYS: -
 Acupuncture
 Homeopathy
 Aromatherapy
 Relaxation techniques (yoga, meditation)

PARKINSON'S DISEASE
  It is chronic neurological motor disorder characterized by progressive degeneration of
dopaminergic neuron in brain stem.it is this deficiency of neurotransmitter dopamine
in brain loading to neurohumoral imbalance between dopamine deficiency and
acetylcholine excess in the basal ganglion causing characteristic signs and symptoms
of Parkinson’s diseases

SYMPTOMS:
 Tremor
 Brady kinesis
 Muscular rigidity
 Weakness
 Expressionless face
 Depression
 Posture imbalance
 Constipation

ETIOLOY:
 Most causes are idiopathic
 Heredity
 Excessive uses of Antipsychotic drug
 Viral inflammation
 Brain trauma stroke
 Arteriosclerosis
 Poisoning by cyanide,Magnase,Carbon monoxide pesticide etc.

DIAGNOSIS:
 Family history
 Review patient symptoms
 CT scan & MRI scan
PATHOPHYSIOLOGY:
Destruction of Dopaminergic neural cells in substantia nigra in the basal ganglia
↓
↓Depletion of dopamine stores
↓
Degeneration of Dopaminergic nigrostrial pathway
↓
Imbalance of excitory (Acetylcholine) and inhibitory (Dopamine) neurotransmitter in the
corpus striatum
↓
Impairment of extrapyramidal tracts controlling complex body movement
↓
Tremor
Bradykinesia
Muscular rigidity

TREAMENT:
PHARMACOLOGICAL TREAMENT
 Dopamine Precursor
Levodopa

 Peripheral Decarboxylase inhibitors

Carbidopa,Benserazide
 COMT inhibitors
Tolcapone,entacapone

 Dopaminergic agonist
Bromocriptine , Ropinirazole,pramipexole
 Glutamate Antagonist
Amantadine
 MAO-B-inhibitors
selegiline,Rasagiline
 Anticholinergics
Trihexyphenedyl,procyclidine
 Anti-histamine
Orphenadrine , promethazine
NON-PHARMACOLOGICAL TREATMENT
 Meditation & relaxation techniques
 Occupational therapy
 Physical therapy
 Speech therapy
 Take olive oil, seafood’s, wine, wholegrain, dairy products and enough water
 Avoid taking saturated food processed, foods, large amount of proteins, sugary foods
&drinks, alcohol.
ALZHEIMER'S DISEASE (AD)
 Is a type of dementia that affect memory, thinking, behaviour It is most common
neurodegenerative brain disorder, starts slowly and it progressively worsen .

SYMPTOMS

STAGE: I
 Early (Mild) (2-4yrs).
 Memory problem
 Cognitive difficulties
 Taking longer time in performing daily task
 Wandering and getting lost

STAGE: II
 Middle (Moderate) (2-10yrs)
 Greater memory loss and infusion
 Unable to recall information like address, Mobile number etc.

STAGE: III
 Late(severe) (1-3yrs)
 Loss of ability to respond to Environment.
 Inability to communicate.
 Physical inability Exercise, sitting, swallowing etc.
 Depend on others for care.

CAUSES:
 Early onset AD [younger onset care (<55years)]
 Familial AD.
 3 MUTATION in genes encoding protein involved in amyloid.
 Plaque formation
Amyloid precursor protein (APP)

Presenilin-1
Presenilin-2-genes
 Non- Familial AD, onset 65 years older.
 Accounts for most cases.
 Increasing age in risk factor for
 Non- Familial AD.
  OTHERS:
 CVD
 Head trauma
 Smoking
 Dietary antioxidants
 Alcohol
 Exposure to pesticides.
PATHOPHYSIOLOGY: -

Cholinergic hypothesis → oxidative stress hypothesis → hyperphosphonylated TAV

protein
Synthesis

(Reduction in Ach E) →Free radical production → extracellular deposition of amyloid

proteins

Neuronal loss atrophy in temperofrontal cortex

Inflammation β-amyloid plaques neurofibrillary

tangles

Alzheimer’s disease
DIAGNOSIS:
 Family history (Asking person or family).
 Medical history.
 Brain scan.
 CT, MRI, PET.

TREATMENT:
PHARMACOLOGICAL TREATMENT
 1st treatment address underlying biology
ADUHELM (aducarumab - Avwa)infusion.
Cognitive Symptoms
 Cholinesterase inhibitors
Donepazil,
Rivastigmine,
Galantamine.
 Glutamate Regulators
Memantine
Non- Cognitive symptoms:
 Antipsychotics
olanzapine
Risperidone
 Anti-depressant-
Citalopram,ericitolopram
 Anticonvulsant
Valporic acid

NON- PHARMACOLOGICAL TREATMENT:

 Take omega -3 fatty acid like first 2 to3 times per day.
 It slow down development of cognitive deficits.
 Take Walnuts that contains protein, vitamins, omega -3 fatty acids, folic acid,
thiamine, vitamin E.
 Take apple, spinach, Extra Virgin olive oil, grape juice, Red wine.

STROKE:
(CVA-cerebro vascular accident)
Stroke occurs when to blood supply to part of the brain in interrupted on reduced. Preventing
brain tissue from getting oxygen nutrients, brain cells begins to die in minutes

They are 2 types:

ISCHEMIC STROKE:-
 About 87% of all stroke are ISCHEMIC stroke, in which blood flow to the brain is
block due to blockage of arteries

HEMORRHAGIC STROKE:-
 nearly 12-13% occurs and caused by leaking on bursting of blood cells in the brain
SYMPTOMS:-
 Sudden numbers or weakness in the face, arm or legs especially in one side of the
body
 Sudden conclusion, sudden speaking on difficulty understanding of speech
 Sudden trouble seeing one or more both eyes
 Trouble walking, dizziness, loss of balance, loss of consciousness, co- ordination
 Severe headache
ETIOLOGY:
 High blood pressure
 Tobacco, smoking
 Physical in- activity and poor diet
 Heart disease
 Diabetes
 Hyperlipidemia
 Age above 60 years
DIAGNOSIS:-
 EEG
 ECG
 MRI
 CT Scan
 Carotid Doppler
 Complete blood count

PHATHOPHYSIOLOGY:-
ISCHEMIC STROKE

Vascular occlusion → cerebral blood flow→ O2 & glucose↓

↓
Alteration of cell membrane

Necrosis Apoptosis

Inflammation

HEMORRHAGIC STROKE

Rupture of blood vessels

↓
Release of blood component into brain

↑ICP Neuron inflammation Oxidative stress Cerebral vasospasm Brain Edema

Neurological dysfunction

TREATMENT: -
PHARMACOLOGICAL TREATMENT:-
Acute ischemic stroke:-
  Ant platelet drug
Aspirin , clopidogrel
 Tissue plasminogen Activator
Alteplase
 Anti-coagulant
Warfarin ,Heparin
 Anti-hypertensive
Labetalol
 Stain therapy

Hemorrhagic stroke:-
 Calcium channel blockers
Nimodipine
 Carotid stinting

NON - PHARMACOLOGICAL TREATMENT:-

 Speech therapy
 Physiological therapy
 Stroke rehabilitation
 Physical therapy
 Occupational therapy
 Avoid smoking and alcohol
 Reduce over weight

MIGRAINE
 Migraine is the common neurological disorder that causes variety of symptoms
most notably throbbing, pulsing, headache and one side of the head.
 Migraine to likely get worse with physical activity lights sounds or smells.
AURA:-
Aura is the group of sensory, motor and speech symptoms that usually act like
warming signals that a migraine headache is about to begin, Aura symptoms are reversible
that produces following symptoms.
 Seeing bright flashing dots, sparkles or lights
 Blind spots in your vision
 Numbness are tangling
 Speech changes
 Ringing in your cars ( tinnitus)
 Temporary vision loss.
PHASES OF MIGRAINE:
 Prodrome→ ( pre headache or premonitory phase)
It's lost few hours too headache
 Auraphase →( can lost has longest 60 minutes to few hours )
 Headache ( It lost 4 hours to 72 hours It is start on one side of your head and spread
to other sides
 Postdrame→ ( It goes on for a day or 2 days it's often called as migraine hangover.
It takes above 8 to 72hours to go though if 4 stages)
SYMPTOMS:
 Sensitivity to lights noise &odours
 Nausea and vomiting
 Abdominal pain
 Loss of appetite
 Difficulty speaking sleeping, visual distribution, neck pain , stiffness in ability, to
concentrate
 Tiredness
 Felling very warm or cold
ETOLOGY:
 Emotional stress
 Missing a meal
 Sensitivity to specific chemical and preservative in foods
 Caffeine (over use)
 Daily uses of pain relieving medication
 Hormonal changes in women's
 Light (flashing, fluorescent lights, lights from TV or computer)
 PATHOPHYSIOLOGY:-
Genetic neurochemical & hormonal factors
↓
Dysregulation of cortical and brain stem excitability
 ↓
Cortical activation → Nociceptive activator
Via peripheral ↓
Trigeminal Vascular changes
Pathway ↑Blood brain barrier permeability
↓
Brain stem activation → Central sensitization
↓
Pain (migraine)
TREATMENT:-
PHARMACOLOGICAL TREATMENT:-
ABORTIVE THERAPY:-
 Non-specific treatment - Ibuprofen, Aspirin, Paracetamol, Diclofenac
SPECIFIC TREATMENT:-
 Ergot alkaloids
Ergotamine, Dihydroergotamine
 5-HT receptor agonist
sumatriplan,Rizatriplan
PREVENTIVE THERAPY :-
 βeta-blockers
Propranolol
 Tricyclic antidepressants
Amitriptyline
NON - PHARMACOLOGICAL TREATMENT:-
 Resting in a dark, quite and cool room
 Applying a cold compress on your forehead on behind your neck
 Massaging in your head
 yoga
 Meditation
GASTRO INTESTINAL DISORDER
GASTRO OESOPHAGEAL REFLUX DISORDER
 GERD is reflux disorder in which mucosa is damaged by reflex of gastric contents in
the oesophagus
SYMPTOMS:-
  Heart burn
 Nausea , bad breathe
 Trouble breathing
 Dysphasia
 Vomiting
 Lump in through
 Lingering cough
 Laryngitis
 Sleep problem
 Asthma that comes on suddenly or get worse.

STAGES:-
STAGE 1:-MILD
This characterized by mild or regurigitation so it's leads to mild inflammation in lower
part of oesophagus.
STAGE 2:- MODERATE
Symptoms will occur several times a week so, it includes heart burn, chest pain, filling
the lump of the throat
STAGE 3:- SEVERE
Severe inflammation in the oesophagus symptoms may include, heart burn,
Regurgitation, sore throat, chronic cough.

STAGE 4:- OESOPHAGUS CANCER

Oesophagus cancer or pre cancerous lesions .it will cancer oesophageal strictures,
oesophagus cancer
CAUSES:-
 Frequent acid reflux
 Obesity
 Pregnancy
 Connective tissue disorder
 Delayed stomach empty

Factors that aggravate acid reflux in rate

 Smoking
 Eating meals
 Eating late night
  Eating fried or fatty food
 Drinking beverages such as alcohol or coffee
 Take medication to such as aspirin

PATHO PHYSIOLOGY:-

Due to any condition like histopathological attraction in LES (or) Upper GIT

↑sed pressure in the Lower oesophageal Sphincter (LES) ↓sed pressure in oesophageal
↓ ↓
Inability of LES to dose properly after Gastric content from high pressure
Oesophageal Content enters into Stomach (stomach) more into Lower [Oesophagus]

Reflux or gastric content into oesophageal through the LES

↓
Irritation and inflammation of oesophageal (oesophagites)
↓
Release chemical mediators in response to inflammation
↓
Formation of Scar tissue in oesophagus. (Oesophageal strictures)

DIAGNOSIS:-
 Upper endoscopy
 Oesophagus manometer
 Symptoms evaluation
 Physical evaluation

TREATMENT:-
 H2 receptor antagonists blocker - -
 Ranitidine
Famotidine
Cimetidine
 Proton pump inhibitor
Esmoprazole
Omeprozole
Lansprazole
Pandaprazole
 Sodium alginate

 Antacid

Milk of magnesia Al2OH gel

 Post agalantine analogous

Misoprosta

 Ulcer protective sucralfate

NON –PHARMACOLOGICAL TREATMENT:-

 Avoid large meals
 Avoid acidic foods such as citric, tomato, alcohol, caffen, chocolates.
 Decrease fat intake
 Avoid lying down within 3-4 after a meal stop smoking.

PEPTIC ULCER DISEASE (PUD)

 Peptic ulcers are source that develop in the lining of stomach lower oesophageal or
small intestine or duodenum.
It’s characterised in three parts:-

1. Gastric ulcer (Ulcer inside the stomach)

2. oesophagus (ulcer inside the oesophagus)
3. Duodenum (ulcer inside the upper part of Small intestine)

SYMPTOMS
 Epigastric abdominal pain
 Weight Loss
 Plotting, pelching, Nausea and vomiting
 Heart burn
 Anaemia
 Dark, Tarry stools
 Hematemecis

CAUSES:-
 Smoking
 H-e coli bacteria pylori infection.
 Pain relieving
 NSAID’s Medication.
 Spicy Foods
 Stress

DIAGNOSIS:-
 Endoscopic procedure
 Urea breath test
 Stool Examination

PATHOPHYSIOLOGY:-
Predisposing factors:-
1. Age (40-60)
 2. life style changes.
3. stress
4. Irritating foods

Damaged to mucosa with alcohol abuse Smoking use of NSAID →1

↓
Acid and prepsinogen release and response to increased stress →2
↓
Infection with Helico bacter pylori →3
↓
Damage mucosal barrier
↓
Imbalance of Aggressive and defensive factor
↓
Low Quality of Mucous
↓
Infection gives increased gastric and decreased somatostatin production
↓
Erosion gastritis
↓
Mucosal ulceration, possible bleeding, scaring
↓
Damage mucosa could that secrete enough mucus to act as barrier against acid
↓
Severe ulceration

TREATMENT:-
PHARMACOLOGICAL
  H2 receptor blockers
Ranitidine,
Famotidine,
Cimetidine

 Proton pump inhibitors

Esmoprazole
ome prazale
Lansoprazole

 Anti H pyloric drugs -Triple Therapy

Metronidazole
Amaxyicillin
Clarithromycin sodium alginate gel

 Antacids
Milk of magnesia, Al₂ OH gel

 Ulcer protective
Sucralfate

 Post agalantine analogous

Misoprostol

NON- PHARMACOLOGICAL TREATMENT:

 Avoid smoking & alcohol
 Avoid Spicy Food, Caffeine
 NSAIDS should be avoided
 Wash your infection hands frequently to avoid infection
 Maintain healthy Lifestyle and eat balanced diet.

ALCOHOLIC LIVER DISEASE (ALD)

  ALD is the result of over consuming alcohol that damages the liver, leading to build
up of fats, inflammation and scaring which could be fortal , ALD is damage of liver
and its function due to alcohol abuse.
SYMPTOMS
 Jaundice
 Edema or swallowing of liver limbs
 Build up of fluid in the abdomen known as ascites
 Fever and sheving
 Ichiy skin
 Clubbing
 Loss of weight
 Blood in vomit and stool
CAUSES
 It is caused by drinking too much alcohol they are 2 ways alcohol misuse can cause
ALD.
 Drinking large amount of alcohol in short amount of time (bring drinking)can
causes fatty liver disease and alcoholic hepatitis.
 Drinking more than recommended limits of alcohol over many years can causes
hepatitis or cirrhosis
TYPE:-
 Alcoholic fatty liver
 Alcoholic hepatitis
 Alcoholic cirrhosis
PATHOPHYSIOLOGY:-
Chronic ethanol intake
↓
Acetaldehyde produce

NADH production lipid per oxidation

↑sed hipogenesis ↓sed FA oxidation Hepatocyte injury

Oxidative stress

Fatty liver Hepatocyte injury

ALD
PHARMACOLOGICAL TREATMENT:-
 Alcoholic abstinence
Naltrexone -500mg/day
Disulferam -500mg/day
Topiramate
Beclofen

NON PHARMACOLOGICAL TREATMENT:-

 Avoid alcohol and smoking
 Weight loss
 Eat a healthy diet low in salt
 Get vaccinated for disease such as influenza, hepatitis a, hepatitis b and
pneumococcal pneumonia
 Liver transplantation option for patient suffering from cirrhosis

INFLAMMATORY BOWEL DISEASE (IBD)

  Inflammatory bowel disease is group of intestinal disorders that cause prolonged
inflammation of the digestive tract. To most Common inflammatory bowel diseases
are:
 Ulcerative colitis
 Crohn's disease.
ULCERATIVE COLITIS
 It is a disease that cause mucosal inflammation and sores (ulcer) in Linning of the
Large intestine (Colon)
CROHN'S DISEASE
 It is chronic relapsing inflammatory disease of the GIT affecting any site from gut
through anus
SYMPTOMS:-
ULCERATIVE COLITIS
 Aldered bowel movement, Increased stool Frequency than decreased stool
Consistency.
 Abdominal pain- Left Lower quadrant Stool
 Scramping
 (Blood in stool) Hematochezia.
CROHN'S DISEASE
 Alderned bowel movement
 Chronic or noctural diarrhea.
 Abdominal pain -post prandial, Right Lower quandrant cramping.
 weight Loss
 Fever.
ETIOLOGY-
 Genetic
 Smoking
 Infection
 Appendectomy
 Stress
 Diet - fat intake, fast Food defective barrier functions.
DIAGNOSIS:-
 Stool examination
 Blood examination
 Imaging and endoscoping

PATHOPHYSILOGY:-
 Triggering events
↓
Dysregulated inflammatory and immune response in genetically susceptible persons
↓
Amplification of immune response
↓
Release of inflammatory mediators
↓ (release of TNF-α pro inflammatory)
Mucous breakdown /and continuous exposure to lumen dietary or bacterial antigens
↓
Impaired handling of microbial
↓
Inflammation

Loss of fine vascular pattern Inflmmation+subsequent injury of

tissue(cryptitis)
↓ ↓
Increased mucosal friability Crypt abscess influx + epithelial necrosis
↓ ↓
Ulceration, exudates, psedopolyps focal aphthoid ulceration
↓ ↓
UC (ulcerativecolitis) Transmural inflammation
↓
Lymphedema and bowel wall thickening
↓
CD (Crohn’s disease)

TREATMENT:
 Aminosalicylates
  Anti inflammatory agents
5 aminosalicylic acid
Mesalamine
Sulfasalazine
 Immunity modifies thiopurines
Azothioprine
Mercaptopurine
 Calcineurin inhibitor
Cyclosporine
 Methotrexate
 Antibiotics
ciprofloxacin
Metronidazole
 Corticosteroid
Methylprednisolone
Hydrocortisone
 Oral-prednisone
Budesonide
 Biologics
Anti TNG agent
infliximab
Adalimumab
NON PHARMACOLOGICAL TREATMENT: -
 Avoid smoking, alcohol consumption
 Avoid use of NSAID'S
 Take more omega-3fatty acid in diet.
 Take fiber rich diet.

HAEMATOLOGICAL DISORDERS
 Involve the blood and include problems with red blood cells white blood cells and
platelets bone marrow Lymph nodes and spleen

IRON DEFICIENCY ANAEMIA

  It is the deficiency of RBC due to insufficient iron intake or poor absorption of
iron in the diet
 Anaemia the blood HB level is below 13g/100ml in men and 12g/100ml in
women.
SYMPTOMS: -
 Headache
 Dizziness
 Fatigue
 Tinnitus
 Palpitations
 Dyspnoea or exertion
 Paler of skin or mucous
 Inflammation sourness of tongue
 Brittle nails

ETIOLOGY
 Persistent bleeding
 Loss of blood due to stomach ulcer or colan, rectal cancer.
 Insufficient iron in diet poor absorption of iron from the diet crohn's disease

PATHOPHYSIOLOGY
Shortage of elemental iron in body
↓
Our bone marrow needs iron to make hemoglobin
↓
Without adequate iron body can’t produce enough hemoglobin for RBC
↓
Decrease haemoglobin is result in insufficient oxygen delivery to the issue

DIAGNOSIS
 Low serum ferritin level -20< mg/L
 Low MCV (Mean corpuscular volume)
 Low MCHC (Mean corpuscular haemoglobin concentration)

TREATMENT:
PHARMACOLOGICAL TREATMENT:
ORAL IRON PREPARATION
Ferrous sulphate -325mg TID
Ferrous fumarate -0.2g TID
Ferrous Gluconate-0.6TID
Ferric ammonium citrate-1g TID
PARENTRAL IRON PREPARATION
Iron dextrar
Ferric carboxymaltose
Iron sorbitol
Iron sodium gluconate

NON-PHARMACOLGICAL TREATMENT: -
 Iron rich diet
 (good sources of iron includes meats,beef,pork, liver and other organ meals)
 (poultry like chicken duck liver)
 (Fish like shellfish) and (Leafy green of cabbage family, broccoli,kale,Turnip
greens).

MEGALOBLASTIC ANAEMIA
  Megaloblastic anaemia is the type of anaemia characterized by formation of
unusually large, abnormal, immature RBC, called as megaloblastic they the
bone marrow, which are released in the blood.
TYPES: -
 Vitamin B12 deficiency
 Megaloblastic anaemia
 Folit deficiency
 Megaloblastic anaemia.

SYMPTOMS: -
 Shortness of breath
 Muscle weakness
 Abnormal paleness of skin
 Loss of appetite
 Weight loss
 Tingling sensation in hands &fit
 Numnus, extremities
ETIOLOGY: -
 Vitamin B12 deficiency
 Folate deficiency
 Mal absorption
 Intestinal disorder are surgery as the stomach
 Alcohol abuse redarts absorption of folic acid.

DIAGNOSIS
 Peripheral blood smear test
 Bone marrow biopsy
 Routine blood count
 Serum folic acid
 Serum cobalamin

PATHOPHYSIOLOGY
Lack of vitamin B12 allows folic acid to be trapped as non - functional methyl tetra hydrafolit
↓
So deficiency of functional FH4 causes impairment of formatt of deoxythymidine
monophosphate(THP). Which is needed for DNA synthesis
↓
As the result large proerythroplast fails to divide rapidly to make mature RBC rather
immature precursors of erythrocyte (Blast cells) appeared to cause megaloblastic anaemia.

TREATMENT
(Vitamin B12 deficiency)
Oral dose of vitamin B2 Supplements (1-10 microgram/day)
For patients with malabsorption dose should be 1000 microgram/day.
Parenteral vitamin B12 (100-1000 microgram) is give -in Im (or) deep SC (subcutaneous).

FOLIT DEFICENCY
Oral folic acid 5mg for day for 15 days when followed by qmg/day

NON PHARMACOLOGICAL TREATMENT

 Megaloblastic anaemia caused by a lack of folate may be treated with oral or
intravenous folic acid supplements.
 Dietary changes also help boost folate leaves more foods to incorporate into
your diet include.
 For vit-B12:- Egg, chicken, red meat, milk.
 Folate deficiency:-Leafy green vegetables, peanuts, oranges.

INFECTIOUS DISEASE
TUBERCULOSIS:-
  Tuberculosis is the communicable infectious disease caused by mycobacterium
tuberculosis.
 Infection spread through airborne droplets breathed into air by person infected in Tb.
SYMPTOMS:-
 Cough testing more than 3weeks
 Coughing up blood or mucous
 Unintentional weight loss
 Night sweats
 Loss of appetite
 Fever
 Fatigue
 Chills
ETIOLOGY:-
 Primary cause of the Tb Mycobacterium tuberculosis it's is small aerobic, no-
motile bacteria bacillus.
 Mycobacterium tuberculosis complex includes four other Tb causing
Mycobacterium.
 M.bovis
 M.africanum
 M.microti
 M.canetti.
DIAGNOSTS:-
 Chest x-ray
 Tuberculin(Montoux)test
 Sputum examination
 Culture test

PATHOPHYSIOLOGY:-
STAGE:-I
Inhalation of airborne droplets containing Mycobacterium tuberculosis
↓
Travel through the respiratory tract to alveoli airways
↓
Engulfment of activated alveoli macrophages, dendritic cells
STAGE:-II ↓
Replication of Mycobacterium tuberculosis
↓
Bursting of cells, release of bacilli-entrance into the other cells
↓
Local pro-inflammatory response (Requirement of mononucleus and DCs)
↓
Infected macrophages, DCs spread to lymph nodes (LNs)
STAGE:-III ↓
T-cells activator in LNS-initiation of cells medicated immunity (CMI)
↓
Migration of activated T-cells
↓
Formation of granuloma

Liquification of granulomas Containment of Mycobacterium tuberculosis

↓ (Dormant bacilli)
Neutrophil influx
↓ ↓
Primary TB Latent TB infection

TREATMENT:-
1st line drugs
 Isoniazid
Rifampicin
Pyrazinamide
Ethambutol
Steptomycin
2nd line drug fluoroquinoloes
(Para amino salicylic acid)
Levofloxacin
Moxifloxacin
Ofloxacin
Cycloserine
Kanamycin
Capreomycin.

NON PHARMACOLOGICAL TREATMENT:-

 Follow the all precaution (wearing the mask, sterilize the hand
etc.) Prior to any activities.
 Take the nutritious diet and make diet chart as per the
instruction by the physician.
 Regular check-up and advice of physician is most important
factor for the treatment of tuberculosis.
 Follow the daily routine (sleep and awake) and try to practice
regular yoga and pranayama.

PNEUMONIA: -
  Pneumonia Lower respiratory tract infection that affects Lungs is which
Alveoli filled makes with. Pus and Fluid which difficulty breathing
SYMPTOMS:-
 Fever chills,
 Shortness of breath
 Protective cough
 Fatigue Trachypnoea

ETIOLOGY: -
Bacteria:
 Staphylococcus pneumonia
 Legionella pneumophila
 Staphylococcus aureus
Virus:
 (Influenza virus)

Fungi:
 Pneumocystis Carinii
PATHOP HYSIOLOGY
Infections of Lungs
↓
Inflammatory response initiated
↓
Alveolar edema + Exudates Formation
↓
Alveoli respiratory respirator bronchioles fill with serious exudates blood cells, fibrin, and
bacteria ↓
Consolidation of Lungs

TREATMENT:-
  Antibiotics
Azithromycin
Etarithromycin
Erythromycin
Moxi floxacin
Tetracycline
 Antiviral drugs
Oseltamivir

NON-PHARMACOLOGICAL MANAGEMENTS:-
 Follow the all precaution (wearing the mask, sterilize the hand etc.) prior to
any activities.
 Take the nutritious diet and make diet chart as per the instruction by the
physician.
 Follow the daily routine (sleep and awake) and try to practice regular yoga and
pranayama.

URINARY TRACT INFECTION (UIT)

  Urinary tract infection is an infections of urinary tract which anywhere From
kidney to uraters, urinary urethra. It' defined micro-organism is the Urine.

TYPES
 Lower tract infection
 Cystitis(bladder). Urethritis (urethra)
 prostatitis (prostate gland)
 upper tract infection
 pyelonephritis (kidney)
SYMPTOMS :-
 Lower UIT
 Dysuria
 Urgency
 Frequency
 Nocturia
 Supra pupic heaxiness
 Hematuria
UPPER UTI
 Flank pain fever
 Nausea
 Vomiting
 Malaise
 Burning micturition
 Cloudy, Dark, Strange smelling Urine
 Tiredness

ETIOLOGY/CAUSESE.
 E-coli- It is most Common type
 Staphylococcus,
 Saprophyticus
 protous SPP
 pseudomonas aeruginosa
 klebsiella pneumonia

PATHOPHYSIOLOGY
Acute kidney injury Continuous inflammatory response result in interstitial edema,
nephritis, acute kidney injury
 ↑
Pyelonephritis
(Bacterial ascension and Hematogenous spread infect renal parenchyma causes
pyelonephritis)
↑
Ascension
(Sufficient bacterial Lead bacterial Colonization can lead bacterial ascension throught
ureter)
↑
Uroepithelium penetrations
(Bacterial fimbriae allows for attachment and penetration of Bacterial bladder epithelial cells)
↑
Colonization
(Bacterial Colonization is per urethra ascension via urethra)

TREATMENT:-
(PHARMACOLOGICAL TREATMENT)
 Trimethoprim – sulfamethoxazole

 penicillin – Amoxicillin Ampicillin

 Tetracylines – Doxycycline, Minocycline

 Quinolones – Ciprofloxacin, Levo floxacin

 Nitrofurantoin –Cephalosporins

RISK FACTOR:-
 Aging
 Diabetes mellitus
  Impaired immune system

IN-MALE
 Prostatic hypertrophy
 Bacterial prostates
 Age
IN-FEMALE
 Started urethra contraceptives
 Sexual intercourse, incompletes
 Bladder empty in age.

NON-PHARMACOLOGICAL MANAGEMENTS:-
 Regular hygiene and cleaning are the most important measure to prevent the
UTIs.
 Do the sexual activity by using of the proper protections.
 During the menstruation use the sanitizing sanitary pad.