year 3 exam Q Flashcards
NAME 2 BIOMARKERs which are a measure of inflammation in the body
C-reactive protein is produced by the liver in response to inflammation. its levels increase rapidly in inflammation in conditions such as disease, infections.
prostaglandins are inflammatory pain (that act on smooth muscle) mediators which are biomarkers for inflammation.
prostaglandin
histamine
bradykinin
what is the cause of lymph nodes which are painful when drinking
Hodgkins lymphoma
list questions you would ask a patient which you suscpet has cancer
have you had any bowel or bladder changes recently
has the lymph nodes enlarged since pain started
does your paln go away with sleep or emdication
do you have any persistent coughing
have you had any unusual bleeding or disharge
what are the stages of hypertension
Normal Less than 120 Less than 80
Elevated 120-129 Less than 80
stage 1= systolic 130-139mmhg
diastolic 80-89
lifestyle changes, meds
stage 2= systolic 140+mmhg
diastolic 90+mmhg
more sever, life style changes and blood pressure lowering meds. increase risk of HA , stroke, kidney damage
Hypertensive Crisis (Emergency situation):
Systolic: Higher than 180 mmHg
Diastolic: Higher than 120 mmHg
Interpretation: A hypertensive crisis is a medical emergency
describe the mechanism involved in the renin-angiotensin-aldosterone system and its function in affecting blood pressure.
describe how this system can both increase or decrease blood pressure
the function of this system is to control BP, fluid balance, na+ homeostasis.
stage 1= decrease bp and renal blood flow is detected by the kidneys and renin is released
stage 2=renin acts on angiotensinogen which is produced by the liver and secreted into the blood stream. converted to angiotensin 1.
stage 3=converted to angiotensin 2 via angiotensin-converting enzyme (ACE) which is found in the lungs
stage 4=angiotensin 2 causes vasoconstriction in arterioles, increasing vascular resistance and blood pressure.
angiotensin 2 stimulates the adrenal glands to release aldosterone
stage 5=aldosterone acts on the kidneys where it promotes sodium and water retention and potassium excretion. this leads to an increase in bp and blood volume
stage 6= once increased, negative feedback is provided to the kidneys and they reduce the stimulus for the renin release. this helps maintain blood pressure. this can b impaired by kidneys disease or heart failure
RAAS inhibitors can blodk systems activation
They are a group of medications designed to disrupt different points in this system, primarily to treat conditions like hypertension (high bp) heart failure, chronic kidney disease and post myocardial infarction
They do this to reduce blood pressure, fluid retention and the strain on the heart and the kidneys
what does GERD stand for
Gastroesophageal Reflux Disease
yoru patient presents with new onset epigastric and retrosternal pain. she feels nauseous on occasion which is relieved when eating. pain increases 1-3hours post/ night pain 11-2am where she feels burning in this area. give diagnosis
gastroesophageal reflux disease (GERD) which presents with heart burn which worsens with lying down and spicy food.
peptic ulcer disease
pain relied by eating then return a few hours later is characteristic of ulcer. pain often occurs at night and can cause epigastric pain.
list 4 main symptoms of bowel cancer
change in bowel habits
blood in stool
constiation and urgency to defecate
abdominal pain or discomfit
where does liquefactive necrosis occur most often?
brain
what is the effect of glucagon on blood sugar levels
increase blood glucose levels
opposition to insulin which lowers blood sugar levels
helps maintain glucose homeostasis
20-year old female presents with acute, severe right lower abdominal quadrant pain. identify 4 potential different diagnosis for right lower quadrant pain
ovarian torsion (twisting on the ovary)
appendicitis
around the umbilicus but later migrates to right lower quadrant
ectopic pregnancy (outside the uterus, mc in fallopian tue)
pelvic inflammatory disease from STI
compare and contrast crowns disease and ulcerative colitis including age and demographics, genetic association, cancer risk, location and distribution, clinical features, complications and extra-intestinal manifestation
both are inflammatory bowel disease.
both have a higher risk if a family member has it
crohns disease can affect people of any age but mc is 15-35. it is more prevalent in urban areas. more common for women.
UC is mc in caucasians. mc age is before 30 but can be up to 60yo. more common for men
crohns disease is the inflammation of the gastrointestinal tract that can occur from th mouth to the anus. mc found at the end of small intestine. it can be caused by autoimmune disorders, genetic factors, smoking, infections such as salmonella and some antibiotics which alter the gut microbiome and diet.
UC is an inflammatory autoimmune disease that causes ulcers in the lining of the colon and rectum. it is believed to be caused by genetic factors and autoimmune issues.
clinical feature of crohns= abdominal cramps (right iliac region) post meals, epigastric discomfort, diarrhoea, fever, strictures, fistulae, cobble stoning mucosa or ulceration.
UC= mucosal inflammation and ulcers in the colon and rectum, GI bleeding, abdominal pain, fatigue, fever, wait loss, urgency to defecate.
extra-intestinal crohns
manifestations= arthritis, kidneys stones, fever and skin rash
UC=arthritis, skin issues
complications of crohns= strictures, fistulas, abscesses, intestinal obstruction
higher risk of bowel cancer
UC= sever bleeding, perforated colon, increased risk of colon cancer
medications for IBD are non steroidal anti-inflammatory drugs to reduce inflammation. lifestyle changes like stopping smoking to drinking. extreme case is surgery.
identify possible aetiologies of cor pulmonate and describe pathogenesis of the symptoms associated with the condition
cor pulmonale is the abnormal enlargement of the right side of the heart as a trust of disease of lungs or pulmonary. it can cause right sided heart failure
it can be caused by pulmonary embolism, interstitial lung disease, cystic fibrosis and other conditions like
the lungs diseases such Chronic bronchitis and emphysema (COPD) is the leading cause of cor pulmonale
COPD is a progresive lung disease that can result in pulomary hypertension and lead to cor pulmonate.
chronic bronchitis is long term inflammation of bronchi. this leads to increased mucus production and persistent cough that occurs at least 3 months, wheezing, peripheral oedema, obesity and peripheral oedema
emphysema is the destruction of the alveolar walls and the loss of lung elasticity which leads to decreased SA decreasing efficiency of gaseous echnage. therefore the removal of co2 decreases.
typically it is casted by smoke, and other environmental pollutants. this can cause cor pulmonae. symptoms are shortnesss of breath, chronic cough and wheezing, barrel chest due to hyperinflation of the lungs, cyanosis .
cor pulmonate results from impaired pulmonary blood flow which leads to elevated pressure in the pulmonary arteries. factors which increase this resistance is hypoxia (low o2 levels causing vasoconstriction), inflammation (COPD) and thrombosis or embolism (increased pressure). this increases pulmonary artery pressure on right ventricle causing hypertrophy of the right ventricle which dilates and is less efficient. as the right ventricle continues it becomes overwhelmed and fails, leading to right sided heart failure. this makes blood back up into the venous system affecting liver, abdomen and legs.
what are the primary endocrine glands and vitamins that play a role in bone health?
parathyroid gland, parathyroid hormone. this regulates calcium in the body by stimulating osteoclast activity to resorb bone and release calcium. promotes activation of vitamin D
Thyroid gland can release t3 and t4 to regulate metabolism of bone cells and regulate actibyt of osteoblasts and osteoclasts
your patients is 30 year old, plays football and has recently recovered from a tibia/fibular fracture. she has her plaster removed and complains of posterior knee pain. it is red and inflamed and sore to touch. patient is taking oral contraceptive birth control pill. what condition are you most concerned about the patient might be experiencing? include reasoning
deep vein thrombosis
patient has recently had a fracture which likely required immobilisation which is a known risk factor for dot as it can cause stasis of blood flow in the veins, particularly in lower expetemities.
posterior knee pain indicates DVT in popliteal vein.
it presents with localised pain, swelling, tenderness in affected area.
oral contracpetive are associated with an increased risk of thrombosis (blood cots). they increase oestrogen which can contribute to hyperocagubility which increases risk of DVT
Redness anf inflammation could be related to post injury symptoms of DVT are similar.
an ultrasound would enable the diagnosis of the DVT .
It could potentially be a bakers cyst however, I would be more concerned with a DVT because it is potentially life threatening as it could turn to a pulmonary embolism if the blood clot was transported around the body.
identify an endocrine hormone which can be associated with arthritis and generalist muscle weakness.s. name the endocrine gland which produces the hormone and a disease associated with the hormone.
cortisol which is produced by the adrenal glands is a steroid hormone which has anti-inflammatory affects. but chronic high levels can affect muscles bone and joints.
it is associated with cushings syndome where there is chronic overproduction of cortisol.
chronic elevated cortisol can lead to arthritis
which gland would have a problem if symptoms are urinary changes
prostate gland
as a part of a skin assessment, observe sin lesions regularly. what does ABCDE refer to when assessing skin lesions.
skin lesions are assessed between benign and malignant tumours or neoplasms.
A= is it asymmetrical, benign tumours are symterical whereas malignant are not
B= borders. does the tumour ahve a border? benign do, malignant don’t have a clear border and can blend into the skin.
C=colour. being tumours are consistent in colour whereas malignant tumours may be darker or lighter. malignant also may have red line sin due to a blood supply.
D=diamter. benign tumours are smaller than 6mm. malignant have a greater diameter usually.
E=evolution. benign tumours do not grow in size rapidly whereas malignant tumours do. if you notice a lesion has grown in the appoint this is a red flag as it can indicate malignancy.
describe virchows triad
there are 3 contributing factors that cause a blood clot, making up the Virchow’s triad.
- endothelial injury. damage to the lining of the blood vessel, underlying tissue is exposed to the blood stream which activates platelets and coagulation.
Causes are atherosclerosis formation, hypertension, smoking, trauma or surgery, infla,,action (vascularised or infections)
2.abnormal blood stasis. this can disrupt normal circulation leading to an increase risk of clot formation due to reducing the clearance of clotting factors.
causes= prolonged immobility, heart failure (reduced CO), irregular heart beat, pregnancy (pressure of uterus on veins) obesity and varicose veins
3.hypercoagubilty= increased tendency to form a blood clot from genetic disorders of external factors. it can result in a thrombus formation.
causes= pregnancy, oral contraceptives, dehydration, genetic mutations, cancer, chronic inflammation diseases.
Risk factors between theonbisis
DVT
Pulmonary embolism and arterial thrombosis
MEDS:
Compressive stockings to improve blood flow
Physical activaty
Anticoagulants
Thrombolysis drugs
Surgery
describe the process of a blood lot formation
1.vasoconstriction
after injury a blood vessel will construct to reduce blood flow to the area to limit blood loss
2.platelet plug formation
platelets are attracted to the site of injury, activated by exposed collagen and other components
platelets stick to exposed collagen and are activated, releasing chemicals like ADP, serotonin which attract more platelets to the area. they forma temporary platelet plug, covering the area to reduce bleeding
3.coagulation cascade
intrinsic pathway= clotting factors are activated by collagen at the site of injury. extrinsic pathway=
tissue factors are released from damaged tissues, activating clotting factors.
both pathways lead to activation of factor x which is crucial in coagulating as it produced thrombin
4.fibrin mesh formation
thrombin converts fibrinogen to fibrin. fibrin strands weave through the platelet plug t strengthen ot. fibrin ,ash traps rbc, abc and platelets to seal the wound
5.clot retention and repair
clot retracts as platelets shrink to bring wound edges closr
growth factors are released to promote healing of the vessel wall
6.fibrinolysis
plasmin breaks down fibrin and dissolves the clot via fibrinolysis. ensures blood vessel is restored to normal function without clot obstructing blood flow.
give a diagnosis for a heart for a man 60 year old with stage 2 hypertension
coronary artery disease is where the coronary arteries become narrowed or blocked due to the buildup of plaques, can cause anigma (chest pain) myocardial infraction or Heart failure.
Primary caused is atheroscler osis by high cholesterol, high bp, diabetes, smoking, unhealthy diet , gtenetuic, chronic inflammation from RA or lupus
hypertensive heart disease
chronic high bp puts strain on heart leading to heart enlargement and thickening of heart muscle and eventually heart failure
Provide an example of a cardiovascular exam to underule any cardiovascular conditions. provide examination routines, reasoning behind symptoms, examination procedures and expected findings given this patient.
pt has chronic lbp
no exercise
raised bp 145/85
systolic 130-139
diastolic 80-90
I would like to conduct a heart exam to rule out any heart conditions such as atrial firbilation where the hearts upper chambers beat irregularly, or any arythmia, pulmonary fibrosis, congestion and pulmonary oedema (fluid accumulation in the lungs, specifically alveoli).
I would then observe if there was any shortness of breath, cyanosis, pallor and any oedema. if there was any chest scars that woud indicate a thoracotomy or sternatomy. I would check patients axillar both sides for lateral thoracotomy. I would check muscle tone ensuring it is equal on both sides. I would observe the chest for any chest walll deformities or signs of a pace maker.
hands-i would assess patients hands for colour, pallor and cyanosis which is an indictor the body isn’t receiving enough o2. cyanosis is a sign of congenital heart disease or heart failure. I would look for splinter haemorrhages in the nail which is a sign of vasculitis and tar staining (smokers). I would ask my patient to perform the scharmroth window test and place their dip’s of the first phalanges together. this would convey clubbing for any underlying CV disease. I would also assess for xanthomas (hypercholestrolaemia).
I would then assess the temperature of both arms and hands and blood pressure bilaterally to rule out subclavian steel syndrome (sends blood to arm instead of brain). I would assess for collapsing pulse by assessing the radial pulse and lifting the arm in the air, a knocking sensation would indicate aortic valve regurgitation.
I would assess the carotid artery by asking pt to hold their breath and listen with the stethoscope for a bruit. I would assess the pulses character and volume. I would assess the jugular venous pressure also.
face: I would observe face for cyanosis, pallor. I would look for anemia in the whites of the eyes and look into their mouth for a high arched palate, their dental hygiene and central cyanosis. I would look at the neck for lymph nodes and traps to rule out pan coast tumour. I would assess the eyes for cornea arcus (outer grey ring ) which can indicate high bp, cholesterol and atherosclerosis. furthermore I would look for Xanthelasma which is the yellow cholesterol deposits around the eys.
palpation: I would palpate the areas I want to asculatet and percuss to assess if there is any inflammation. this could be teethes syndrome or chostocondritis which would affect the effectiveness of the heart exam, restricting rib mobility.
percussion: I would percussion to rule out any fractures or tenderness and it would allow me to listen to any changes in sound which could indicate a pulmonary oedema.
ascultate:i would listen to the diagrpahm and the bell of the stethescpr to hear high and low pitched sounds and any murmurs. I will listen for any crackles to rule out pulmonary fibrosis. I would listen to all the valves in the heart: right 2nd intercostal space for aortic valve, left 2nd intercostal space for pulomic valve , left 4th intercostal space for tricuspid valve and then left intercostal space in the mid clavicular line for mitral valve.
describe a respiratory exam
I would perform this exam to assess conditions such as asthma or COPD pulmonary oedema and pulmonary embolism’s.
General inspection:
I would ask pt for consent and assess if there was any shortness of breath, coughing or wheezing.
If breathing diffculty and assessory muscles were used. This is a sign of respiratory distress, asthma, pneumonia and COPD
I would look at the breathing pattern, for tachpynea (rapid more than 20bpm) or bradypnea (slow fewer than 12bpm) or irregular breathing.
Chest deformities for scoliosis, barrel chest which can indfercate underlying lung conditions like COPD or restrictive lung disease
I would assess the pallor, cyanosis, if there was any oedema, the pt lymph nodes and trachea deviation. I would perform the hepatojugular reflex test to assess the jugular venous pressure.
hands: I would assess the hands for colour, tar staining from smoking, finger clubbing using schamroths widow which is a sign of underlying CV disease, joint swelling. Splintered nails as a sign of vascularised. And temperature.
I would assess for a bounding pulse associated with co2 retention and pulsus paradox where pulse wave volume decreases in inspatroy phase. Severe actue asthma and COPD
face: I would observe pt face for congested red face suggestion co2 retention.
I would then asses tone and texture of the chest for symmetry. Can indicate pleural effusion pneumotheiax, cyanosis for poor oxygenation, chest movements. Unequal expansion can suggest pneumothorax and pleural effusion
Palpationb:
Chest expansion test
I would place my hands on pt back at thumbs level of 10th rib and ask pt to take a deep breath. Thumbs should ive apart symmetrically. Unequal is pleural effusion or pneumothorax
I would ask my Pt to say 99 while i palpate the chest. Increased vibration can indicate pneumonia and decreased may suggest pleasurable effusion and pneumothorax.
I would also parapets for tenderness, muscle strain, rib fractures and tietzes syndrome or costchondritis.
PERCUSIION:
I would percuss the supraclavicular, infraclavicular, axial and chest wall.
Normal is healthy, dullness and hyper resonance are a sign of unhealthy lung tissue. Dulles can indicate pleasurable effusion, pneumonia or a mass.
Hyper resonance may be heard with emphysema, pneumothorax.
Would palpate anterior and posterior chest wall and comparing both sides.
Auscultation:
I would all regions of chest, anteriorly and posteriorly. I would assess quality and volume.
Bronchial is harsh sounding which is associated with consolidation,
Quiet breath sounds which suggest reduced air entry to the area of ;uni, pneumothorax and pleural effusion.
Wheeze for asthma, COPD
Strider: high pitched due to turbulent air flow
Coarse crackles:pneumonia, pulmonary odema
Crackles: pulmonary fibrosis.
I
how would you take blood pressure from a patient
preparation:
ensure patient sits comfortably with there back supported and feet flat on floor.
arm should be exposed and relaxed on a flat surface at the level of the heart.
equipment= wrap cuff around upper arm, 2-3cm above elbow. the ‘bladder’ of the cuff should be placed over the brachia; artery.
cuff should be snug.
3=measuring bp.
palpate brachial artery for pulse using 1st and 2nd phalanges
inflate the cuff rapidly to 20-30mmHg above the point where the pulse disappears.
deflate cuff slowly with stethoscope diaphragm placed over the artery.
cuff should deflated 2-3mmhg per second
listen for diastolic (when sounds disappear) and systolic (first appearance of tapping sounds ) pressure and record the reading; systolic over diastolic.
repeat on other arm to rule put subclavian artery stenosis, peripheral artery disease or any abnormalities.
Normal BP:
Systolic < 120 mmHg and Diastolic < 80 mmHg.
Elevated BP:
Systolic 120-129 mmHg and Diastolic < 80 mmHg.
Hypertension Stage 1:
Systolic 130-139 mmHg or Diastolic 80-89 mmHg.
Hypertension Stage 2:
Systolic ≥ 140 mmHg or Diastolic ≥ 90 mmHg.
Hypertensive Crisis:
Systolic > 180 mmHg and/or Diastolic > 120 mmHg. Immediate medical attention is needed.
what is subclavian artery stenosis
narrowing or blockage of the subclavian artery which would restrict flow of oxygenated blood to the arm of the affected side
causes: atherosclerosis which is the build up of fatty plaque inside the artery walls. resulting from high bp, high cholesterol, smoking, diabetes
trauma
congenital heart disease
what is peripheral heart disease
vessels that supply blood to the limb become narrowed or blocked usually due to atherosclerosis
limits circulation
coldness in legs or feet
weak or absent pulse
wounds or ulcers
shiny skin
numbness or tingling
gangrene
treated y statins, blood pressure meds, surgery , lifestyle changes
What is the difference between pneumothorax, pleura effusion and pulmonary odema
Pneumothorax is the presence of air in the pleural cavity which can cause the lung to partially or fully collapse
Causes : trauma like rib fracture
lung disease like COPD, asthma cystic fibrosis
Symptoms: shortness of breath, sudden onse chest pain, reduced or absent breath sounds on affected side, hyper resonance or percussion over affected area
Treatment: can resolve or thoracostomy (chest tube)
Imaging: chest x-ray collapsed lung, air pocket
Pleural effusion is the accumulation of excess fluid in the pleural cavity
Causes: high hydrostatic pressure or low protein
Heart failure, nephrotic syndrome, liver cirrhosis (scarring)
Symptoms: chest pain, shortness of breath (lung compression) decreased or absent breath sounds obver fluid and Dullness to percussion
Treatment:antibiotics for infection or heart failure
Drainage or chest tube
Imaging: chest x-ray fluid in pleural space
Imaging:
Pulmonary odema is the accumulation of fluid in the lungs ALVEOLI, impairing gas exchange
Causes: cardio genie pulmonary odema (often from left sided heart failure)
Symptoms: sudden shortness of breath
Cough producing frothy pink thick mucus
Crackles on auscultation
Cyanosis
Treatment: oxygen therapy
Treating heart conditions by vasodilators
Imaging: chest x-ray haziness bilateral
What is Chronic Obstructive Pulmonary Disease
Progressive lung disease characterised by persistent air flow limitation and respiratory symptoms dye to airway or alveolar abnormalities. Exposures to harmful particles or gases, mc cigarette is leading cause of morbidity and mortality worldwide
Key features:
Chronic and progressive
Airflow limitation : difficulty exhaling due to obstruction of the airways caused by inflammation, narrowing and destruction of lung tissue.
Causes:
Smoking
Environmental exposure
Genetic
Recurrent lung infections
Chronic inflammation leads to narrowing of airways,excess mucus production and damage to alveoli
Air trapped on lungs leading to overinflation
Structural damage like loss of elasticity
Compare and contrast left and right sided heart failure
LSHF occurs when left ventricle fails to pump blood effectively out from the aorta to the rest of the body
Leads to pulmonary congestion and poor systemic perfusion. Low output
RSHF occurs when right ventricle fails to pump blood effectively out pulmonary artery to lungs
Causes systemic venous congestion and fluid build up in peripheral tissues. Systemic venous congestion involving fluid retention.
Causes:
LSHF
Hypertension, coronary artery disease, myocardial infarction, cardiomyopathies, valvular disease like aortic stenosis
RSHF
LSHF mc
Cor pulmonae and chronic lung diseases
Pulomary hypertension
Congenital heart defects
Valvular diseases like tricuspid regurgitation
Symptoms:
LSHF
Dyspnea (shortness of breath)
Difficulty breathing lying flats
Fatigue and weakness
Waking up at night and gasping for air
Pulmonary congestion
Crackles
Cough
RSHF
Peripheral odema
Ascites
Juguyloar venous distension
Weight gain
Hepatomegaly (enlarged liver)
Nausea
Abdominal px
Diagnosis:
LSHF
Echocardiogram to asses ventricular size and function
Chest x-ray to show pulmonary odema and cardiomegaluy
RSHF
Echocardiogram to asses ventricular size and function
Chest x-ray to show pleural effusion or pulmonary congestion
Treatment:
Both diuretics to reduce fluid and congestion
LSHF
Beta blockers
Aldosterone antagonists to reduce fluid retention
RSHF
Treat underlying cause LSHF
Oxygen therapy
Both CO is decreased due to deficiency in blood pumping and decreased oxygenation
Both have reduced stroke volume due to impaired ventricular contraction or increased afterlod/ hypertension,
Less blood is pump0ed into systemic circulation
Both HR Increases (tachycardia) to maintain CO
Both blood pressure increases in (jugular venous distension) due to back up of blood.
What is vasculitis
Inflammation of the blood vessels which can affect arteries, veins or capillaries.
Changes in the walls of blood vessels such as thickening, weaklening, narrowing or scarring. This can disrupt normal blood flow leading to organ or tissue damage,
3 types: large-vessel vasculitis, medium and small
Causes: giant cell arteries t
Associated with infections Hep B/C, cancer (lymphoma) medications or drugs and autoimmune disease like RA
Symptoms:
Fever, fatigue, weight loss, muscle or join pain. Skin rash or ulcers, shortness of breath, cough, nosebleeds, high bp, blood in urine, numbness, abdominal pain, dairohe or bloody stools
Can cause:
Luminal narrowing reducing blood flow, weakening of vessel wall which can result aneurysm or rupture, clot formation (thrombosis)
Diagnosis:
Blood test with inflammatory markers like prostoglandins and C-reactive protein
CT/ MRI
Urine tests
Tissue biopsy
Treatment:
Meds like corticosteroids, immunosurpresents, treating High BP, physical therapy for joint or muscle pain or surgery
What are aneurysms?
Abnormal bulge or ballooning in the wall fo the blood vessel caused by a weakness in the vessel wall
Can allow blood vessel to expand under pressure, increasing risk of rupture.
Can occur in any blood vessel in body mc found in arteries
Can have:
Aortic aneurysm (Abdominal aortic aneurysm AAA)
Cerebral aneurysm
Peripheral aneurysm (popliteal mc, carotid and femoral)
Coronary aneurysm
Causes:
Atherosclerosis
Hypertension
Genetics
Injury or trauma
Infections like sypohillis and endocarditis
Smoking
Synotons:
Dependant upon area
May not cause symptoms
AAA can cause pulsating and when ruptures abdominal pain severe, back pain, dizziness and fainting
Cerebral aneurysm can cause a thunderclap headache, nausea, vomiting, loss of vision and consciousness
Peripheral is pain or tenderness in the aneurysm compressing nearby structures
Swelling or pulsating lump
Thoracic aortic aneurysms
Chest or back pain
Difficulty breathing or swallowing
Cough
Blood clots are root of both aneurysms and embolisms in some form
Diagnosis:
Ultrasound
CT or MRI
Can cause rupture or dissection which is life threatening.
Treatments:
Blood pressure control like beta blockers
Cholesterol lowering drugs
Surgery
Emergency treatment
Lifestyle change like quit smoking, genetic counselling, healthy diet and exercise
compare and contrast systolic and diastolic heart failure
S= reduced ejection fraction due to weakened heart muscles.
left ventricle doesn’t contract efficiently
decreased ability to pump blood out of aorta
often caused by: HA, chronic hypertension, dilated cardiomyopathy, valvular heart disese, coronary artery disease (MC), arrhythmia
D=ejection fraction is reserved. muscle is stuff leading to impaired relaxation and filling. can’t fill adequately reducing blood pumped out
causes:left ventricular hypertrophy, chronic hypertension, aging, diabetes and fibrosis of heart tissue,
symptoms
S=decreased CO, fatigue, dyspnea, difficulty breathing when lying flat, edema, pulmonary congestion
dizziness and fainting
D=pulmonary congestion, fluid buildup, shortness of breath, fatigue, pulmonary dome
Diagnosis:
S=echocardiography shows reduced ejection fraction
D= echocardiography shows preserved ejection fraction
Treatment:
S=angiotensin receptor blockers, beta blockers, diuretics for fluid retention, defirbiltor
often imrpoves
D=controlling hypertension and diabetes
Angiotensin receptors blockers
beea blockers
significant morbidity
what is atherosclerosis and its formation
chronic inflammatory disease of the arteries characterised by fatty plaque deposits
plaque leads to narrowing and hardening of arteries. restrict blood flow and increase risk of HA, strokes, peripheral artery sea
atherosclerotic plaque is made of cholesterol, fat, calcium
stiff arteries increase BP and reduce ability of vessels to dilate
over to,e plaque can become unstable and rupture leading to formation of thrombus
formation:
1.endothelial injury
caused by inflammation, smoking, high bp, diabetes or high cholesterol
- LDL Cholesterol Accumulation’low density lipoprotein’ cholesterol particles penetrate inner layer of the arteries and accumulate in the wall and promotes plaque formation
3.Inflammatory ResponseLDL triggers an inflammatory response. sends WBC to engulf them
4.Formation of Foam Cellsmacrophage attempt to digest but they become overloaded with lipid material and transform to foam cells which contribute to the accumulation of fat and cholesterol in the wall
- Plaque Formation and Fibrous Cap
fatty streak formed in the wall by foam and smooth muscle cells.
smooth muscle cell will proliferate and migrate to site of injury forming a fibrous cap which can stabilise the plaque. if rupture lead to thrombosis
6.plaque growth and calcification
calcium deposits form in plaque, stiffening the artery. reduce lien narrowing blood flow
7.Plaque Rupture and Thrombosis
fibrous cap and become weakening if inflammation is present. clotting factors are release if ruptured leading to thrombus which can cause HA, stroke
risk factors: increase with age
men >
family history and geentics
can cause:
coronary artery disease
carotid artery disease
peripheral artery disease
aneurysms
treatments:
lifestyle
meds like statins, anti platelet drugs, diabetes management
surgery like stenting or a bypass
what is IBS
Chronic gastrointestinal disorders that affects the large intestine(colon) it is a functional disorder of the digestive tract
key features:
abdominal pain, relived after bowel movemet
altered bowl movement
bloating and gas
no strutural abnormalitis
urgency to defecate
fatigue
sleep distubrances
mucus in stool
nausea
classifications:
1.IBS with diarrhoea Frequent, loose stools, often accompanied by urgency or a sense of incomplete evacuation.
2.IBS with Constipation (IBS-C):
Difficulty passing stools, with infrequent, hard, or lumpy stools. There may be straining and a feeling of incomplete evacuation.
3.IBS with Mixed Symptoms (IBS-M):
Alternating episodes of diarrhea and constipation.
4.IBS-Unsubtyped (IBS-U):
Symptoms that don’t clearly fit into one of the above categories.
diagnosis:
rule out iBD, infections and celiac
blood tests, stool test may be perfomed
low FODMAP
increased /reduced fibre
avoid trigger foods
medications like laxatives, anti diarrhoea agents , probiotics, stress managemnet and regular exercise
what is asthma
inflammation and narrowing of the air ways in lungs due to hyperresponsivty of stimuli
chronic, airway inflammation, bronchoconstriction, airway hyperresponsivness (tightening of muscle)
symptoms:
wheezing, shorts of breathe, coughing, chest tightness. she people have exercise induced asthma, increased mucus production. structural changes can occur in the airway walls called airway remodelling. can permanently narrow vessels and more reactive chronic asthma symptoms
causes:
family history, genetic motions, environmental factors like those with allergies increased risk to develop asthma,a. hay fever, eczema
diagnosis:
history of symptoms and family history
physical exam for wheezing
spirometry test for how much air you can exhale after a deep breath to determine restriction
chest x-ray
allergy tests
treatment:
inhaled corticosteroids: reduce swelling and mucus prdution
combination inhalers, leukotriene modifers to block inflammation
allergen avoidance, lifestyle change like quitting smoking, managing stress and staying alive
describe osteoarthritis
degenerative joint disease mc arthritis
protective cartilage wears down over time. bones may become thicker over time and develop osteophytes which can contribute to joint pain and stiffness. synovial fluid can become thinner. inflammation can occur at irritated joint tissues
Risk Factors for OA:
typically affecting people over 50.
Genetics: Family history can play a role in susceptibility
Joint Injury: Previous joint injuries or repetitive stress on a joint can increase the risk of developing OA in that joint.
Obesity: Extra weight puts more stress on weight-bearing joints, such as the knees and hips, which increases the likelihood of OA.
Gender: Women are more likely to develop OA, especially after menopause.
Symptoms:
pain
stiffness
swelling
decreased roms
crepitus
diagnosis:
x-rays and mir can show the joint structure and narrowing or bone spurs
treatment:
no cure
non steroidal- anti inflammatory drugs
lifestyle changes: weight management, activity modification.
corticosteroid injections, hylaraunc acid injections
join replacement surgery
describe rheumatoid arthritis
chronic autoimmune disorder that affects joints, causing inflammation pain and stiffness
unlike OA ra occurs when body immune system mistakenly attacks its own tissues, targeting the synovium. over time leads to inflammation and join damage
symmetrical.
thicken synonym and destroy the cartilage and bone, painful swollen and potentially deformed joinsts
can affect other organs such as heart, lungs, blood vessels and eyes leading to complications like CV disease, lung disease and rheumatoid nodules (lumps under skin)
symptoms: joint pain and stiffness
swelling
fatigue
fever and weight loss
reduced roms
rheumatoid nodules
deformaties (ulnar deviation)
affected joints:
small joints in hands, wrists and feet
same joins both sides of body
risk factors:
genetics HLA-DR4 gene
gender: women 30-60
: smoking can trigger the immune response
family history increases risk
diagnosis:
blood tests for inflammatory markers or rheumatoid factors
imaging tests x-rays, ultrasound, MRI
treatment:
non steroidal anti inflammatory drugs
corticosteroids
pain relievers
physical therapy like exercise
lifestyle changelik diet and rest
surgery for tendon repair, synovectomy, joint replacement
describe osteoporosis
weakened bones that are more prone to fracture
bone mineral density decreases
develops slowly over many years
imbalanced bone remodelling with bone resorption outpacing bone formation
mc fractures in spone, hip and wrists
risk factors:
age 30+
gender women greater risk especially after menopause. oestrogen decrease increasing risk of bone loss
family histryincrease risk
causcauon or asian higher risk
hormone imbalances like hypothyroidism or cushings syndrome more likely
smoking and alcohol increase risk of low body weight
corticosteroids and meds long-term
symptoms:
back pain
loss of height
postural chanhge
fracturs
diagnosis:
x-ray
DEXA scan indicates risk of fracture
treatment:
meds like parathyroid hormone, bisphosphonates slow rate of bone respiration
exercise for weight bearing and strength training
fall prevention
surgery like hip replacement or spinal surgery
describe avascular necrosis
blood supply to a bone is disrupted leading to death of bone tissue.
bone becomes weak an may eventual;;y collapse. e;adomg to pain, joint dysfunction and deformity.
mc hip, knee, shoulder, ankle
risk factors:
trauma or injury, dislocation of hip and femoral head fracturs
steroid use
excessive alcohol consumption which would impair blood flow to bones
HIV/AIDS, gout, lupus. OA, sickle cel disease
obesity, genetics and radiation therapy
symptoms:
pain
limited ROMS
joint stiffness
limp or altere gait
deformity
diagnosis:
x-rays
MRI
CT
Biopsy
treatment:
pain relief
Bisphosphonates: These medications are sometimes used to slow the progression of bone damage by inhibiting bone resorption, although they are not always effective for AVN.
physical therapy
joint protection like using a cane
surgery for bone grafts, hip and knee replacement , total joint fusion, core decompression removing a portion of bone to relieve pressure and increase blood flow
describe osteomyelitis
infection of bone when bacteria, fungi or other pathogens invade bone tissue leading to inflammation, pain and potential bone destruction
can cause ncecoriss, septic arthritis, spread of infection
mc long bones, spine, pelvis
Acute Osteomyelitis: This form develops rapidly, often within a few days to weeks, and is characterized by severe symptoms such as fever, intense pain, and swelling.
Chronic Osteomyelitis: If the infection is not adequately treated, it can lasting for months or even years.bone destruction may occur, and there can be intermittent flare-ups of infection. The infection may also result in the formation of sequestra (dead bone pieces) and fistulas (abnormal channels that connect the bone to the skin)
pathigen is MRSA but can be caused by other bacteria and fungi, especially in immunocompromised individuals.
causes:
athogens enter the bloodstream and travel to the bone from an infection elsewhere in the body. Hematogenous osteomyelitis is more common in children and tends to affect long bones.
Direct Inoculation (traumatic or post-surgical infection):
diabetic foot ulcers
spread from adjacent soft tissue
risk factors:
diabetes
recent surgery or trauma
weakened immune system
poor blood flow
chronic kidney disease
sickle cell disease
symptoms:
acute
pain
fever
swelling
warmth
tenderness
limited ROM
fatigue
nausea and vomiting
chronic:
intermitent pain
swelling
fever
formation of fistula
visible bone defmoty
dead bone
diagnosis: blood test for elevated WBC count, CRP, Blod cultures
x-rays, RI, CT, Bone biopsy
treatment:
amputation,
bone graft
debridemtn (removal of dead bone)
wound care
describe ankylosing spondylitis
chronic inflammatory disease that primary affects the spine or SI joists
progressiv inflammation, joint stiffness and fusion of spine
‘bamboo spine’
causes: HLA-B27
immune system dysfunction
environmental triggers like infections of GI
family history
young adults late teens to early 30s. mc in men
symptoms:
chronic back pain
stiffness 30 min-hours
fatigue
postural changes
pain and swelling in other joints
inflammation of eyes
enthesitis (inflammation of entheses can cause pain achlis tendon, plantar fascia and knees
heart problems
breathing diffucloyies
bowel sykptoms
diagnosis:
x-rays
MRI for inflammatiom
HLA-B27 test
CRP
Treatment:
nonsteroidl anti inflammatory drugs
corticosteroids
physical therapy for spinal flexibility, strengthening muscle and improving posture
exercse
surgery- spinal or joint replacement
list valve disorders of the heart
- Aortic Stenosis (AS):
Description: A condition where the aortic valve becomes narrowed, obstructing blood flow from the left ventricle into the aorta
Causes: Congenital defects, age-related calcification, or rheumatic heart disease.
Symptoms: Shortness of breath, chest pain, fatigue, dizziness, or fainting.
Diagnosis: Echocardiogram, cardiac catheterization.
Treatment:
replacement ( - Aortic Regurgitation (AR) (also called aortic insufficiency):
Description: The aortic valve does not close properly, allowing blood to flow backward into the left ventricle during diastole (when the heart relaxes).
Causes: Endocarditis, rheumatic fever, aortic root dilation, or trauma.
Symptoms: Palpitations, fatigue, shortness of breath, and a characteristic widened pulse pressure.
Diagnosis: Echocardiogram, MRI, or cardiac catheterization.
Treatment: Medical management (e.g., afterload reducers like ACE inhibitors) or valve surgery if severe.
. Mitral Stenosis (MS):
Description: The mitral valve becomes narrowed, restricting blood flow from the left atrium to the left ventricle.
Causes: Most commonly due to rheumatic heart disease, which causes scarring and thickening of the valve leaflets.
Symptoms: Shortness of breath, especially with exertion, fatigue, palpitations, and in severe cases, pulmonary hypertension and right-sided heart failure.
Diagnosis: Echocardiogram, Doppler ultrasound, chest X-ray.
Treatment: Valve balloon valvuloplasty (for suitable patients), mitral valve repair, or mitral valve replacement if necessary.
- Mitral Valve Prolapse (MVP):
Description: The mitral valve leaflets become too large or floppy, causing them to prolapse (bulge backward) into the left atrium during systole.
Causes: Often idiopathic, but can be associated with connective tissue disorders like Marfan syndrome or Ehlers-Danlos syndrome.
Symptoms: Can be asymptomatic or present with palpitations, chest pain, and fatigue. Sometimes associated with murmurs.
Diagnosis: Echocardiogram or ultrasound.
Treatment: For most people, MVP requires no treatment, but those with significant regurgitation or symptoms may need medications or surgical intervention.
tricuspid stenosis
obstructs RA-RV
mitral regurgitation
back flow of blood into LA
pulmonary stenosis
right ventricle to pulmonary artery nerrowing
pulmonary regurgitation
pulmonary valve fails to close into RV
endocarditis
Infection of heart valves by bacteria or fungal infects. bacteria, fungal. antibiotics
rheumatic heart disease
rheumatic fever is an bacterial infection following strep through or scarlet fever. scarring of heart valves leading to stenosis or regurgitation. antibiotics and valve repair or replacement,t
treatment:
anti-inflammatory drugs like beta blockers
lifestyle modification
weight loss, exercise
diuretics to reduce fluid buildup
mitral valve repair or replace,ent
valve repair, mechanical valves or biological tissues
open heart surgery
dietary adjustment like low sodium low fat
regular monitoring
describe pneumonia
infection of the lungs causing alveoli to fill with fluid or pus making it difficult for o2 to reach bloodstream. caused by microorganism, bacteria, fungi or inhaled substances.
bacterial pneumonia, viral pneumonia, fungal pneumonia, aspiration pneumonia
symptoms:
cough with phlegm or mucus, fever, chills, shortness of breath, chest pain and fatigue
sever cases may result in difficulty breathing, confusion, rapid HR, cyanosis
risk factors:
age very young or ederly
weakened immune system
chronic conditions like asthma, diabetes, heart disease, COPS
smoking, recent viral infection which weakens immune system
diagnosis
respiratory exam
x-ray
blood test to identify infection
treatment:
antibiotics
antiviral
anti fungal meds
can get
pleural effusion
abscesses
sepis
respiratory failure
describe pleurisy
pleurisy is inflammation of the pleura. visceral and parietal rub together casing pain especially when breathing, coughing or sneezing
causes:
infections, viral, bacterial or fungal
autoimmune diseases like lupus or RA can cause infllamtion
pulmonary embolism
lung cancer
injury or trauma, pneumothorax
symptoms:
sharp stabbing chest pain worsen with coughing, breathing or sneezing
can radiate to shoulder or back
shortens of breath
dry cough, fever, pleural friction rub which can be hard through stethascope
diagnosis:
chest-cray
ct scan
respiratory exam
blood test WBC count for infection signs
trreatment:
corticosteroids
non steroidal anti inflammatory drugs
antibiotics or antiviraks
treat underlying conditions ie autoimmune diseases
can lead to pleural effusion , chronic pin, infection soread or sepiss
respiratory issues
describe H-P axis
hypothalamic pituitary axis is critical part of endocrine system hat regulates numerous physiological processes like growth, metabolism, reproduction and stress
consists of hypothalamus, pituitary gland and the target organs or glands that they influence through complex network of hormones and feedback loops
target organs include the gonads. ovaries and testes. LH and FSH from anterior pituitary act on the gondads to regulate reproductive function. in females for menstrual cycle and males they involve in sperm production
Adrenal Glands: ACTH stimulates the adrenal cortex to release cortisol and other steroid hormones, which are critical in the body’s response to stress, immune regulation, and metabolism.
Thyroid Gland: TSH from the anterior pituitary stimulates the thyroid gland to produce thyroid hormones (T3 and T4), which are essential for regulating metabolism, energy production, and growth.
Liver and Other Tissues: Growth hormone (GH) from the anterior pituitary affects the liver and other tissues to promote growth, cell regeneration, and the breakdown of fat for energy. It also stimulates the liver to produce insulin-like growth factor 1 (IGF-1), which promotes bone and tissue growth.
feedback mechanism:
negative feedback: the release or a hormone inhibits further production. high levels of cortisol will inhibit the release of ACTH from the pituitary and CRH from hypothalamus. known as the hypothalamic-pituitary-adrenal (HPA) axis feedback loop.
positive feedback: initial hormone release stimulates further release.
he release of GnRH from the hypothalamus during the menstrual cycle, which triggers the pituitary to release LH and FSH. The surge in LH and FSH causes ovulation, and the process is further amplified by positive feedback until ovulation occurs.
disorders are hypopituitarism, hyperituitarism, thyroid disorders and reproductive disorders
Reproductive Function (HPG Axis): The hypothalamic-pituitary-gonadal axis controls the release of sex hormones and regulates reproductive processes such as the menstrual cycle, ovulation, and sperm production.
Stress Response (HPA Axis): The hypothalamic-pituitary-adrenal axis controls the body’s response to stress through the release of cortisol. When the body experiences stress, the hypothalamus releases CRH, which stimulates the pituitary to release ACTH, leading to cortisol release from the adrenal glands.
Growth and Development (GH Axis): Growth hormone regulation by the hypothalamus and pituitary, with GH releasing hormone (GHRH) stimulating the pituitary to release growth hormone, which promotes growth and tissue repair.
describe oesophagitis
inflammation of oesophagus.
mc is gastoesophageal reflux disease (GERD)
acid reflux
stomach acid flows backwards int the esophagus. this can irritate and inflame the lining causing symptoms like hear tburns, regurgitation and chest pain
infections can cause it especially with weakened immune systems. yeast, herpes virus or bacterial infections
medication:
non steroidal anti-inflammatory drugs and some antibiotics can damage the loninong leading to inflammation and ulcers
allergies with an overproduction of WBC causes inflammation in oesophagus associated with food alergies
autoimmune diseases or physical injury or irritation can also cause it
symptoms:
pain or discomfort when swallowing
difficulty swallowing
sore throat
chest pain
heart burn
vomiting nausea
coughing or wheexing
food impaction
diagnosis;
endoscop
biopsy
x-ray
blood tests
treatment:
lifestyle modifications LOW FODMAP
avoiding down after meals
antacids
antibiotics
corticosteroids
pain relief
dietary changes like soft or liquid diet
complications:
strictures
ulceration
perforation
describe ulcers
open sores or lesions that develop o the skin mucous membranes on the body
in the digestive system peptic ulcers are mc
peptic ulcers, gastric ulcers and deudenal ulcers, mouth ulcer and skin ulcer
causes:
H.pylori infection weakens protective mucus lining in stomach or duodenum making it more vulberae to acid damage.
non steroidal anti inflammatory drugs can irritate or damage the stomach lining increasing the risk. NSAIDs inhibit prostaglandins which protect stomach lining from acid
excessive alcohol consumtpim
smoking
stress
symptoms:
bloating and fullness
heartburn
acid reflux
loss of appetie
indigestion
burning stomach pain
can cause perforation, bleeding or gastric outlet syndrome
diagnosis:
endoscopy
blood tests
stool tests
x-ray
breath test
treatment:
antacids
antibiotics
avoiding NSAIDS
reducing alcohol intake, quitting smoking, managing stress , surgery
complications:
internal bleeding, cancer, perforation, gastric outlet obstruction
describe constipation
common digestive issue infrequent difficult or painful bowel movements.
fewer than 3 bowel movies per week. hard dry stool, a sensation of incomplete evacuation or abdominal discomfit
1.primay constipuation
non medical condition but lifestyle factors or problems with colon
low fibre diet
inadequate fluid intake
lack of physical activity
changes in routine
ignoring the urge to have a bowel movement
- secondary constipation
underlying medical conditions affecting bowel function
meds: antidepressants, antacid and iron supplements, opioids can slow bowel motility
neurological conditions like spinal cord injuries, parkinsons
hypothyroidism
diebets
IBS
Colon or rectal disorders
pregnancy
other diseases lie kidney or liver ideas
stress and anxiety can often alter gut motility by increasing muscle tension
symptoms:
infrequent bowel movements
hard or Lumpy stools
abdominal pain or discount
feeling of incomplete evacuation
nausea
diagnosis:
rectal exam
blood tests
x-rays c scans
colonoscopy
treatment:
dietary changes, increase fibre intake, limit processed food, adequate hydration
excise meds like fibre suplimets , stool softeners , laxatives , treating underlying conditions like iBS, Diabetes or hypothyroidism
or colostomy and surgery
describe appendicitis
inflammation of the appendix, can lead to life threatening infection called peritonitis
causes:
obstruction of the lumen mc, feral matter, lymphoid tissue, intestinal worms
infections , trauma or injury
family history, age, or certain infections (e.g., viral infections of the gastrointestinal tract) may increase the risk.
symptoms:
abdominal pain around belly button but may go to lower right of the abdomen and sharp
tenderness
nausea and vimiting
loss of appetite
fever
constipation or diarrhea
difficulty passing gas
risk factors:
age mc 10-30
gender mc men
family history
infection
diagnosis:
blood test for elevated WBC
urine tests
imaging ike ultrasound, cT scan, MRI
treatment:
surgery like appendectomy
antibiotics drainage
non-surgery
complications:
ruptured appendix
abscess formation
sepsis
regions and Ddx of GIT
Right Hypochondriac:
Location: Upper right part of the abdomen, just below the ribs.
Key Organs: Liver, gallbladder, right kidney, part of the colon.
Conditions:
Cholecystitis (gallbladder inflammation)
Hepatitis (liver inflammation)
Peptic Ulcer Disease (if the ulcer is in the duodenum)
Right Kidney Stone (renal colic)
Epigastric:
Location: Upper middle part of the abdomen, just below the sternum.
Key Organs: Stomach, pancreas, part of the duodenum.
Conditions:
Gastritis
Peptic Ulcers (gastric or duodenal)
Pancreatitis
Gastroesophageal Reflux Disease (GERD)
Left Hypochondriac:
Location: Upper left part of the abdomen, just below the ribs.
Key Organs: Spleen, stomach, left kidney, part of the colon.
Conditions:
Splenic Enlargement (splenomegaly)
Gastritis
Left-sided Pleuritis
Pancreatitis (left-sided)
Right Lumbar (Flank):
Location: Middle right side of the abdomen.
Key Organs: Ascending colon, right kidney.
Conditions:
Appendicitis (in the early stages)
Renal Colic (kidney stones)
Diverticulitis (right-sided, though rare)
Umbilical:
Location: The center of the abdomen, around the navel.
Key Organs: Small intestine, part of the colon.
Conditions:
Intestinal Obstruction
Gastroenteritis
Umbilical Hernia
Mesenteric Adenitis (swollen lymph nodes in the mesentery)
Left Lumbar (Flank):
Location: Middle left side of the abdomen.
Key Organs: Descending colon, left kidney.
Conditions:
Diverticulitis (left-sided)
Renal Colic (left-sided kidney stones)
Constipation (particularly in the descending colon)
Right Iliac:
Location: Lower right part of the abdomen.
Key Organs: Appendix, cecum, right ovary (in women).
Conditions:
Appendicitis
Ovarian Torsion (in women)
Ectopic Pregnancy (in women)
Cecal Diverticulitis
Hypogastric (Pubic Region):
Location: Lower middle part of the abdomen, just above the pubic bone.
Key Organs: Bladder, uterus (in women), small intestine, part of the colon.
Conditions:
Urinary Tract Infection (UTI)
Bladder Infections/Calculi
Endometriosis (in women)
Irritable Bowel Syndrome (IBS)
Left Iliac:
Location: Lower left part of the abdomen.
Key Organs: Sigmoid colon, left ovary (in women).
Conditions:
Diverticulitis (left-sided)
Ovarian Cysts/Torsion (in women)
Constipation (in the sigmoid colon)
List 9 abdominal regions
- Right hypochondriac
Liver, gallbladder, R kidney, SI
(Gallstones, stomach ulcer, pancreatitis)
2.Epigastric region
Stomach, liver, pancreas, duodenum, spleen, adrenal glands
(Stomach ulcer, pancreatis, gall stones, indigestion)
3.left hypochondriac
Spleen, colon, left kid, pancreas
(Stomach ulcer, duodenum ulcer, pancreatis)
4.r lumber
Gall;aider, liver, r colon
(Kidneys stones, urine infection, constipation, lumbar hernia)
5.umbilical region
Umbilical, SI, duodenum
(Pancreatis, appendicitis, stomach ulcer, IBS)
6,L lumbar
Descending colon, left kid
(IBD, kidney stones, constipation)
7.R iliac
Appendix, cecum
(Appendicitis, pelvic pain, constipation, groin pain)
8.Hypogastric region
Urinary bladder, sigmoid colon, femal reproductive organs
(Urine infection, appendicitis, pelvic pain, IB)
- L iliac
Descending colon, sigmoid colon
(Pelvic pain, groin pain, inguinal hernia)
Aims of inflammation (4)
Bring immune cells to the area
Destroy pathogens
Remove cellular debris
Begin repair
describe vascular phase of acute inflammation
initial respone to injure or infection. minutes-hours.
1.vasodilation
Proinflammatory mediators like histamine, bradykinin, and prostaglandins cause the smooth muscle in the walls of arterioles to relax, leading to vasodilation
increase blood floe to the affected area causing redness and heat
2.increased vasular permedabilty
Inflammatory mediators, such as histamine, bradykinin, and leukotrienes, increase the permeability of the endothelial cells lining the blood vessels. This can lead to gaps forming between endothelial cells.
allows plasma protein to leak and immune cells to surrounding tissues. selling.
3.exudation of fluid
The leakage of fluid, proteins, from the blood vessels into the interstitial space leads to the formation of exudate—a fluid rich in proteins, white blood cells, and debris.
swelling. dilute toxins and pathogens
4.stasis and margination of leukocytes
increased blood flow and changes in vessel permeability lead to the slowing of blood flow, a process known as stasis.
describe the cellular phase of an acute response
following vascular phase.
1.leukocye recruitment
immune cells like neutrophils and macrophages are recruited to set of injury by chemitaxis.
cytokines like IL-8 compliment proteins and bacterial prodyctes signal guide immune cells along a conc gradient to site of infection
margination occurs and cells line up against the endothelium. these cells then role and p-seecton on endothelial express and interact with leukocytes facilitating rolling and adhering. leukocytes adhere to the endothelial
diapedesis occurs an leukocytes migrate out of the blood vessel and Ito surround tissue via diapedesis. via CHEMOTAXIS
Once the leukocytes, especially neutrophils and macrophages, have reached the site of infection or injury, they engage in phagocytosis
if inflammation is successful the inflammatory response wills tob. macrophages fear apoptic neutrophils and other debris. if not clear, inflammation can be chronic leading to ongoing tissue damage and recruitment of t lymph and fibroblasts.
Compare acute vs chronic inflammation
Acute inflammation onset is immediate whereas chronic is delayed.
Acute duration is a few days whereas chronic is up to months and years
Causative agents for acute is bacteria and injured tissues whereas chronic is persistent acute inflammation, viral autoimmune
Acute major cells are neutrophils, basophils, monocytes, macrophages whereas chronic is mononuclear, mono, lymphocytes, plasma cells, fibroblast
Acute primary outcomes are resolution, abscess formation and chronic inflammation. Chronic outcomes are tissue destruction, fibrosis, necrosis
describe the process of innate immunity
the bodys first line of defence against pathogens. non-specific . present from birth and is rapid.
Bacteria with antigen on surface releases endotoxins
Endotoxins act on mast cell nucleus to release inflammatory cytokines
Stimulating P-selectin on endothelial cells to initiate extravasation
Transmigration, margination, adhesion, diapedeasis and positive chemotaxis occurs
The inflammatory cytokines act on endothelial cells causing them to contract and increase permeability (swelling)
Smooth muscle cells are acted on and they relax leading to vasodilation and heat and redness
Neutrophils undergo exocytosis of free antigens. Apoptosis
Macrophages undergo phagocytosis forming a phagolysosome
MCH2 recombination and attach to specific antigen and present on cell membrane
Macrophage turns into antigen presenting cell
Complimentary pathway is activated
Classical
Alternative
Lectin
Allowing chemoattract more neutrophils and macrophages to the area
Opsonisation(pathogens are marked for destruction)
Cell lysis
Inflammation enhances by activation of mast cells
Interferential Alpha, beta, gamma stimulate neighbouring cells / macrophage toi increase in size and number
Describe the process of humoral response
Free antigen binds to b lymph
MCH2 and b cell receptor form an antigen presenting cell
Macrophage binds to t-h cell via CD4 protein and tcell receptor
Differentiation of th cell into
Th1
Th2 (IL 2,4,5)
IL 4 + 5 send chemical messages to b lymph to stimulate cell proliferation = clinal expansion
B cell differentiation into memory b cells for long term protection
Plasma cells which secrete antibodies which cause neutralisation or opsonisation
Innate vs adaptive
Innate is non-specific and targets all pathogens whereas adaptive is highly specific
Innate immunity response is immediate within minutes to hours. Adaptive is delayed and days to weeks
Innate there is no memory as same response is repeated to exposure whereas adaptive has memory so is faster, stronger response
Duration of innate is short term defence, adaptive is long lasting
Key cells innate is phagocytes (macrophages, neutrophils), natural killer. Adaptive is B-cells, t-cells
Name 3 cells involved in immune response and their roles
Macrophages engulf and digest pathogens and are antigen presenting allowing T cells to be activated in adaptive immune repsonse
TH cells- release cytokines that activate other immune cells like B cells to produc antibodies and CT cells to kill infected cells
B cells for humoral immune response. Differentiate to plasma when activates which produce antibodies to neutralise pathogen or marking them for destruction by other immune cells
Name 3 antigen presenting cells
Macrophage-phagocyte
Dendritic cells- activate T cells
B-cells-present to ht cells
Describe GI practical assessment
Observation of age, any confusion, pain, scars, abdominal distension, pallor, hernias, odema, hyperpigmentation
Hands:
Pallor, finger clubbing, temperature, radial pulse, any hair loss, xanthomas, splintered nails, tar staining, dupuyrtens contracture
Face: xasnthelasma, cornea arcus, anemia, mouth for cyanosis, dental hygiene an high arched palette.
Chest for any scars, inflammation, hailer loss, gynaecomastia and spider nevi. Cullens sign which is bruising inferior to belly button for haemorrhaging and umbilical hernia, grey turners sign which is flank (side) bruising herniation.
Auscultation:
Tinkling bowel sounds which is associated with bowel pobstruction
Absent bowel sounds suggests ileus
Aortic brutis 1-2cm superior to umbilicus. Associated with Abdominal aortic aneurysms
Light palpation
Liver: percuss upwards from right iliac fossa, 1-2cm a time, resonant
to dull.
• Spleen: percuss from right iliac fossa to left costal margin noting resonance to dullness.
• Bladder: Percuss downwards from umbilicus from resonance to dullness
Note any rebound tenderness, guarding and masses,
Deep palpation for size, location, shape , mobility, pulsatility
Palpate clockwise from the right hypochondriac.
Palpate viscera
Liver
Start at the right iliac fossa using your finger pads
Ask patient to take a deep breath
Work upward to right costal margin
Assess for size, consistency, tenderness, pulsatility, degree of extension below
costal margin
Causes of hepatomegaly:
Hepatitis, carcinoma, metastasis, leukaemia,
glandular fever, tricuspid regurgitation, haemolytic anaemia
Gall bladder: : Not normally palpable in a healthy person ( gall stones, pancreatic malignancy. Infection)
Location: R costal margin, mid-clavicular line (large, well defined mass that moves
with respiration)
Murphy’s sign: Pain mid-breath on palpation indicates cholecystitis
Spleen: Only palpable if x3 its size (splenomegaly). Begin palpating at right iliac
fossa and progress to left costal margin.
Causes of splenomegaly; liver cirrhosis, haemolytic anaemia, CHF, splenic
metastasis, glandular fever.
alpation of the viscera
Ballot the kidneys:
R Kidney:
- R hand at anterior abdominal wall just below the right costal margin
- L hand behind the patients ribs, below the flank
Palpable indicates polycystic kidney disease,, cancer
Aorta:
Bilateral hands, superior to umbilicus in the midline
Hands should move superiorly
If hands move outwards: AAA
Describe Hodgkin’s lymphoma
Cancer originating in the lymphatic system
Affects lymphocytes, abnormal growth
Presence of an abnormal cell called Reed-Sternberg Cells
Cancer disrupts the normal function of the immune system
Risk factors:
Age- 15-35 and 55+
Family history increases risk
Epstein-Barr virus increases risk
Weakened immune system HIV/AIDS
Symptoms:
Enlarged non-tender lymph nodes
Fever
Night sweats
Weight loss
Fatigue
Itchy skin
Pain IN LYMPHNODES AFTER DRINKING ALCOHOL
Diagnosis:
Physical exam, biopsy with Reed-Stenberg cells to confirm diagnosis
Imaging CT, MRI
Blood tests for infection
4 stages
1- one lymphoid node
2-involving 2 lymph regions on same side of diaphragms
3-both sides diaphragm
4- affecting other organs
Treatment:
Chemotherapy, radiation therapy, stem cell transplant , immunotherapy
High cure rate. 5-year survival rate
Describe non-hodgkins lymphoma
Originates in lymphatic system
B cells are most commonly affected by can affect T cells top
Tumours cab grow into other organs
Disseminates wildly
Risk factors:
Age, mc in adults 75< 30%
HIV/AIDS
Infections like Epstein-Barr virus
Having a family member increases risk
Chemical exposure
Chronically inflammation like RA
Symptoms:
Swolllen, painless lymoph nodes
Fever
Unexplained weight loss
Night sweats
Fatigue
Abdominal pain or swelling (spleen or liver is involved)
Shortness of breath or cough (if affects the chest)
Diagnosis:
Physical exam
Biopsy
Imaging CT/MRI
Blood test for atrial cell counts
Treatment: chemo, radiation therapy, immunotherapy, stem cell transplant, targeted therapy
Describe acute lymphatic leukemia
Cancer affecting blood and bone marrow
Rapid production of immature WBC (Lympohoblasts)
impairing the body’s ability to fight infections, carry oxygen, and control bleeding.
B-cell mc, can affect T cell
Risk factors:
Mc children
Genetic mutations like Down syndrome
Family history
Chemical exposure
Previously cancer treatment
Viral infections Epstein Barr virus
Symptoms:
Fatigue
Fever
Frequent infections
Paleness
Shortness of breath
Pains in bones or joints
Swollen lymph nodes
Enlarged spleen
Bleeding from gums and nose
Purple bruised mucous membrane
Diagnosis:
Blood test for abnormal WBC, RBC
Bonemarrow biopsy
Imaging X-RAYS CT
Treatment:
Therapy
Stem cell or bone marrow transplant
Targeted therapy
Immune therapy
High survival rate for children especially
90% 5 year
Describe chronic lymphocytic leukemia
Affects blood and Bon Māori
Slow-growing
Abnormal B-lymphocytes are dysfunctional and don’t fight infections
Naive lymphocytes
Risk factors:
Age mc 60
Men>
Family history
Genetic mutations
Exposure to chemicals]
Immune system conditions like RA
Symptoms:
May not have noticeable symptoms
Swollen lymph nodes
Fatigue
Unexplained weight loss
Frequent infections
Fever
Abdominal discomfort
Night sweats
easy bleeding and bruising
Diagnosis:
Blood tests high number of lymphocytes
Bone marrow biopsy
Imaging: CT or ultrasound
5 year survival rate 83%
Describe Polycystic Ovary Syndrome (PCOS)
: One of the most common hormonal disorders in women of reproductive age (approximately 5-10% of women).
Causes: An imbalance of reproductive hormones leads to irregular ovulation, which can cause cysts to form on the ovaries.
Symptoms: Irregular periods, excess hair growth (hirsutism), acne, obesity, thinning hair, and infertility.
Complications: Increased risk of diabetes, heart disease, and endometrial cancer.
Treatment: Hormonal birth control to regulate periods, lifestyle changes (diet, exercise), medications to manage symptoms like hair growth or acne (e.g., anti-androgens), and fertility treatments for those who want to conceive
Describe endometriosis
Affects about 10% of women of reproductive age.
Causes: endometrium grows outside the uterus, usually on the ovaries, fallopian tubes, or other organs within the pelvis.
Symptoms: Severe pelvic pain, painful periods, pain during sex, infertility, and heavy or irregular menstrual bleeding.
Complications: Infertility, chronic pain, and adhesions (scar tissue) in the pelvic region.
Treatment: Pain management (NSAIDs), hormonal therapies (birth control, progestin), surgery to remove excess tissue, and in severe cases, hysterectomy.
Describe pelvic inflammatory disease
Common among women of reproductive age, particularly those with untreated sexually transmitted infections (STIs) like gonorrhea or chlamydia.
Causes: Bacterial infections that ascend from the vagina or cervix to the uterus, fallopian tubes, and ovaries.
Symptoms: Lower abdominal pain, fever, abnormal vaginal discharge, pain during sex or urination, irregular menstrual cycles.
Complications: Chronic pelvic pain, infertility, and ectopic pregnancy (a pregnancy outside the uterus).
Treatment: Antibiotics to treat the infection. In severe cases, surgery may be needed to remove infected tissue.
Describe ectopic pregnancy
Prevalence: Occurs in about 1-2% of pregnancies.
Causes: When a fertilized egg implants and grows outside the uterus, usually in a fallopian tube.
Symptoms: Abdominal pain, vaginal bleeding, dizziness, or fainting (signs of a ruptured ectopic pregnancy).
Complications: A ruptured ectopic pregnancy can lead to severe internal bleeding and can be life-threatening.
Treatment: Medication (methotrexate) or surgery to remove the ectopic pregnancy.
Describe ovarian cancer
The fifth most common cancer in women and the deadliest gynecologic cancer.
Causes: Risk factors include family history of ovarian or breast cancer (BRCA1/BRCA2 mutations), age (most cases occur after age 50), and reproductive history (e.g., women who have not had children).
Symptoms: Abdominal bloating, pelvic or abdominal pain, difficulty eating or feeling full quickly, frequent urination.
Treatment: Surgery, chemotherapy, and sometimes targeted therapies.
Describe colon cancer
Colorectal cancer
Begins in large intestine (colon) or rectum. Starts as a polyp on the inner lining
Risk factors:
Age 50<
Family hostile y
Genetic factors
Diet high red meat, low fibre
IBD
Lifestyle, lack of physical activity, smoking, excessive alcohol consumption
Symptoms:
Change in bowl habits
Blood in stool
Abdominal pain or cramping
Unexplained weight loss
Fatigue or weakness
Anemia
Diagnosis:
Colonoscopy
Fecal blood test
Biopsy
Treatment:
Chemo
Surgery
Radiation therapy
Prevention:
Regular screenings
Healthy diet
Excessive
Reducer Tabasco and alcohol
List the hallmark signs of cancer (8)
Sustaining prolifertaive signals
Evading growth supressor
Resisting cell death
Enabling replicative immortabilut
Inducing angiogenesis (blood vessel; growth)
Activating invasion and metastasis
Deregulating cellular energetic (Warburg effect increased glycolysis)
Avoiding immune destruction
Describe stomach cancer
Cancer in the mucosa
Mc is adenocarcinoma
Risk factors:
Age mc 60
H Pylori infection
Diet with high salt, smoked, pickled foods and low in fruits and veg
Family history
Smoking
Chronic gastritis
Genetic factors
Symptoms:
Indigestion and heartburn
Bloating
Stomach pain or discomfort
Nausea and vomiting
Loss of appetite
Unexplained weight loss
Diffulty swallowing
Fatigue
Diagnosis:
Biopsy
CT/MRI, ultrasound
Blood tests
Treatment:
Surgery
Chemotherapy
Radsiation therapy
Targeted therapy
Immunotherapy
Describe breast cancer
There are several types
Symptoms:
Lump or mass in the breast
Unexplained changes in size, shape or appearance of the breast
Skin changes like redness, dimpling or thickening
Unusual pain in breast
Nipple discharge
Risk factors:
Women>
Age 50+
Family hstory
Genetic mutation BRCA2 BRCA1
Hormonal features like eagerly or late menopause
Lifestyle factors like obesity, physical inactivity, alcohol, smoking
Diagnosis:
Mammography
Ultrasound
Biopsy
MRI
Treatment:
Surgery
Radiation therapy
Chemotherapy
Hormone therapy
Targeted therapy
Immunotherapy
Describe prostate cancer
Adenocarcinoma
Risk factors: age 50 mc over 65
Family history
Race- mc in African American men
Genetic factors BRCA1 BRCA2
Diet and lifestyle
Symptoms:
Frequent urinatioj
Difficulty starting or stopping urination
Weak or interapputed flow
Blood in urine or semen
Painful ejaculation
President pain in lower back, hips, pelvis
Erectile dysfunction
Diagnosis:
Digital rectal exam
Biopsy
Imaging tests MRI, CT, ultrasound
Treatment:
Surgery
Radiation therapy
Chemotherapy
Immunotherapy
Target therapy
List main endocrine disorders and describe them
Diabetes Mellitus:
1. Autoimmune disorder where body’s immune system attacks and destroys the insulin producing beta cells in pancreas
2.resistance to insulin. Obsesity and lifestyle factors
Hypothyroidsism
Hyperthyroidism: Graves’ disease
Cushing syndrome high level of cortisol
Addisons disease nt enoug cortisol and aldosteroneby the adrenal glands
Polyvystic ovary syndrome
Hormone disorder. Poilycystic ovaries
Hyper/hypoparathyroidsm calcioum levels in blood
Acromegaly excess GH
Hypoglycaemia low blood sugar levels imbalance of insulin or hormones
Describe lymphangitis
Infection of lymphatic cells, bacteria, virus and fungi.
Skin or deeper tissues, cut wound or inset bite
Cellulitis is mc
E.coli
Symptoms:
Red streaks
Pain and tenderness over affected area
Fever and chills
Swollen lymoph nodes
Genera;l malaise
Skin affects
Diagnosis:
Blood test for elevated WBC
Cultures
Imaging like CT
Treatment:
Antibiotics
Penicillin
Pain re;Eid
Elevate limb
Complications:
Abscess formation
Sepsis
Chronic ly,opahtc duystdntion like lymphoedema
Describe lymphadenitis
Inflammation of infection of lymph bnodes
Lymph node infection Vida bacteria, virus or fungi
Cat scratch, TB, sinus infection or dental abscess, infected wound, HIV, Adenovirus, parasitic, RA, cancer like leukemia
Symptoms:
Swollen lymph node
Pain and tenderness
Redness and warmth
Fever anc chills
General mailiase
Night sweat s
Pus drainage
Weight loss
3 Types
Acute, chronic, suppurative (severe)
Diagnosis:
Blood tests for elevated WBC
Imaging like CT
Biopsy
Treatment:
Antibiotics like pen icilis, antivirals for Epstein-bar vrs
Antifungals
Drainage of abscess
Pain management
Compliactaionbs:
Sepsis
Abscess formation
Lymoph drainage issues
Describe ischameia
Reduced or restricted blood flow to a tissue or an organ leading to a shirteage fo o2 and nutrients
Results in tissue damage, dysfunction and necrosis
Mc with thre heart , brain and limbs
Causes:
Atherosclerosis
Thrombosis
Embolism
Vasospansm
Low bp
Compression
Torsion or tweaking
Infection or inflammation like vascularised
Symptoms:
Pain
Weakness
Pale of cool skin
Numbness or tingling
Edema
Organ dysfunction like HA
Myocardial ischameia is MI , ches pain, dizzy, sweat, shirt breath
Cerebral ischameia (brain) lead to stroke, weakness of numbness in face, arm or leg. Vision loss and balance loss
Peripheral: peripheral artery diastase. Weak pulse pain during exercise
Treatment: thrombolytics, anticoagulants, surgery, lifestyle change fo diabetes, high cholesterol, no smoking
Complications:
Stroke, HA, renal failure
Organs dyscfuntiuon
Necrosis
Gangrene
Describe infarction
Necrosis caused by interruption of blood supply
Metabolic waste products can’t be removed
Causes:
Thrombosis
Atherosclerosis
Embolism
Vasospasm
Trauma
Hypotension
Compression
Infections endocarditis
Types: Red (Hemorrhagic) Infarction:
occurs when the affected tissue is supplied by a single blood vessel, and the blockage causes the blood to back up into the tissue, leading to bleeding.
It is often seen in venous infarction, where blood flows into the tissue but cannot drain, causing congestion and bleeding. It is also seen in pulmonary infarctions or infarction in tissues with a dual blood supply (such as the lungs, liver, and intestines).
often seen in organs with a rich collateral blood supply (such as the lungs), where the obstruction may result in bleeding into the affected area.
White (Anemic) Infarction:
occurs when the affected tissue has a single, end-arterial blood supply (i.e., no alternative collateral circulation). The lack of blood flow results in pallor or paleness (anemia) in the tissue. commonly seen in solid organs with a single arterial blood supply, such as the heart (myocardial infarction), kidneys (renal infarction), and spleen (splenic infarction).
Causes pain, MI, organ dysfunction, swelling, shock,
Mc type is myocardial infarction. Blockage of one or more coronary armies
Cerebral infarction (stroke) , pylomary infarction , renal
Diagnosis: CT or MRI, chest x-ray , blood tests for elevated cardiac enxymes, biopsy
Treatment:
Bypass surgery
Thrimbilytics
Anticoagulation
Surgical removal
Describe cell cycle
G1 Phase
Interphase
Cell grows and metabolises, protein synthesis and energy porodution
Cell prepares for DNA replication, checking for damage (G0 non dividing if damaged)
CHeckpoint
S phased
DNA replication by dna polymerase enxyme
2 sister chromatids connected by a centromere
Chromosome duplication - 2 chromatids
G2 phase
Cell growth and preparation for mitosis
Checkpoint to ensure it is correct
M phase (mitosis)
Prophase
Nuclear envelope breaks for, spindle
Metaphase. Align at equator spindle fibres attach at centomemer
Anaphase sister chromatids are pilled apart to opposite poles
Telophase de condense and nuclear envelope reforms around each set of chromosomes
Cytokinesis: dividing of cytoplasms into daughter cells
Describe cellular immunity
Cell-mediated immunity
dendritic cells, macrophages encounter and digest pathogens
Antigen is displayed with Major histompatibility complex
Dendritic cells or macrophages enter lymph node
T cells with rejectors specific to antigen bind to APC
Cytocic t-cells via CD8
T cells via CD4
They recognise the antigen complex and bind.
Stimulators signals are required for full activation of thr T-CELL
Once activated, clonal expansion occurs where T cell rapidly divides to procure clones. Large population of activated T cells specific to the pathogen
Th1 promote inflammation and activation of cytoxic t calls and macrophages to fight intracellular pathogens
Th2 release IL4,5 activate B cells for antibody production
CD8 cytoxic T cells are activated and release performing and granzymes undergoing apoptosis
Formation of memory T cells for long term immunity
Once pathogen is cleared immune system downregulates to suppress activity
