CSB520 Final Exam LOI

Explain the impact that renal failure has on the rest of the body (cardiovascular, skeletal, haematological)

Cardiovascular

- no kidney filtration --> acidosis (removes H+, decreases pH) --> increase in potassium in blood --> cardiac arrhythmias

- Overactivation of RAAS --> increases vascular resistance (BP) and water absorption (BV) --> systemic hypertension --> LSHF --> RSHF

Skeletal

- loss of kidney response to PTH --> no VD activation --> decreases Ca absorption by blood, Ca lost in urine --> break down bones to release Ca --> renal osteodystrophy + soft tissue calcification

Haematological

- decrease EPO --> anaemia

- acidosis (decreases pH)

List the main malignancies that affect the male and female urinary system

Both

- nephroblastoma

- renal cell carcinoma

- transitional cell carcinoma

Male

- prostate (adenocarcinoma)

List causes of glomerulonephritis & possible consequences

Cause - blood born stimuli

Consequences (bilateral) - chronic kidney failure

Why is the renal papilla susceptible to toxic injury and ascending infections

- Papilla = tip of renal pyramid projecting into the calyx

Ascending infection: first bit of the kidney proper where bacteria is gonna hit as it goes from the lower UT, causing necrosis

Toxic injury: urine is the most concentrated before leaving the kidney and entering the calyx, therefore if there is something toxic in the urine, the papilla is susceptible to injurry

List the major differences between ascending & descending infections

Ascending = coming up, likely to only affect one kidney, or part of one kidney

Descending = via the blood, more likely to affect all functional units in both kidneys and lead to renal failure

Why are UTIs (ascending infections) more common in cis-females than cis-males

- shorter urethra

- urethra closer to anus

- no prostate

- greater risk of trauma in the urinary system

- mucosal changes in reproductive system can predispose to UTIs

List the possible causes and consequences of urinary stones

Causes: stasis of urine, infection, pre-existing stones, dehydration, calcium metabolism disorders, gout

Consequences: pain, haematuria, hydronephrosis (obstruction of urine flow), predisposed to infection, encouraged stone formation , chronic irritation

List some causes of hydronephrosis

Unilateral - stone, tumour, scar tissues contracting

Bilateral - enlarged prostate gland, cancer impacting bladder walls, scar tissue contracting, foreign objects inserted into urethra

Describe the innate defences in the conductive region of the lungs

1. sneezing

2. coughing

3. mucociliary clearance system

Describe the innate defences in the respiratory region of the lungs

macrophages

Describe the pathogenesis of the 2 most common primary lung cancers

1. Goblet cells --> hyperplasia (mutation) --> dysplasia --> carcinoma in situ --> adenocarcinoma

2. Simple ciliated --> metaplasia (smoking) --> stratified squamous --> dysplasia --> carcinoma in situ --> squamous cell carcinoma

Why are the lungs a common site for secondary cancers

- lungs receive all venous blood for reoxygenation, blood flow is a way of metastasis

How are the lungs affected by LSHF

- pulmonary congestion = increased hydrostatic pressure = pulmonary oedema

How do lung diseases contribute to RSHF

- lung disease --> scarring/obstruction --> pulmonary hypertension = RSHF

- pulmonary emboli --> resistant blood flow --> pulmonary hypertension = RSHF

Where do most pulmonary emboli travel from

DVT --> superior vena cava --> RS heart --> lungs

Define bronchiectasis (COPD)

irreversible and progressive dilation of the bronchi and bronchioles

- causes: smoking, obstruction, infection

- consequences: predisposes to other COPD, pulmonary failure, respiratory failure, RSHF

Define chronic bronchitis (COPD)

persistent productive cough lasting at least 3 months and in 2 consecutive years

- causes: smoking

- consequences: predisposes to other COPD, pulmonary failure, respiratory failure, RSHF

Define emphysema (COPD)

irreversible and progressive destruction of alveolar walls without obvious fibrosis

- causes: chronic bronchitis, asthma, coal dust, smoking, genetics

- consequences: predisposes to other COPD, pulmonary failure, respiratory failure, RSHF

Define bronchial asthma (COPD)

chronic inflammatory disorder, hyper reactive airways, causing bronchospasms due to smooth muscle contractions

- atopic: immune system overreacts to antigen

- non allergic: hyperirritability of bronchial tree

What type of reaction occurs in atopic asthma

type I hypersensitivity response

What happens in acute vs chronic atopic asthma

Acute

- bronchoconstriction

- swelling in wall

- increase mucus production

Chronic

- hypertrophy of muscle = thicker, more powerful, responsive walls

- hyperplasia of goblet cells = impacts mucociliary clearance system

What is pneumoconiosis, which particles are commonly implicated in Australia, and what can they cause

chronic inflammation caused by the inhalation of particulate matter

- particle: caol, asbestos, silica

- consequence: loss of functional tissue, wasting, pulmonary hypertension, RSHF, risk of cancer

What is pneumonia

infection that inflames air sacs, causing them to fill with fluid/pus

Differentiate between lobar and bronchopneumonia

Lobar

- high virulence

- can affect anyone

- rare

- throughout lungs

- acute inflammation

Bronchopneumonia

- low virulence

- opportunistic infection

- affects immunocompromised

- common

- occurs in patches within the lungs

- acute inflammation

Type I Diabetes Aetiology

an autoimmune disease, where beta cells are destroyed by their immune system = no beta cells = no insulin production

Type II Diabetes Aetiology

can be genetic, but also influenced by environment, insulin insensitivity in target organs, take up enough glucose to function, but not enough to decrease blood glucose

Type I Diabetes Pathogenesis

- target tissues cannot take up blood glucose without insulin = starving = alternate fuel sources (fatty acids/ketones)

- high blood glucose due to target tissues not using it

= hyperglycemia, polyuria, ketoacidosis, underweight

Type II Diabetes Pathogenesis

- if lifestyle changes aren't made, beta cells burn out = irreversible condition

= overweight, truncal adiposity, polyphagia, polydipsia, polyuria, neuropathy

Type I Diabetes Treatment

Insulin

Type II Diabetes Treatment

Weight loss

Long Term Effects for Both Diabetes Types

Atherosclerosis = neuropathy, nephropathy, retinopathy, ischaemic heart disease

Understand what is meant by 'functional' tumour & the possible implications for hormone levels

well-differentiated, still producing the hormone but in an uncontrolled way

- leads to excess of the hormone

What is the most common cause of hyperthyroidism

Grave's disease (autoimmune)

symptoms of hyperthyroidism

- reduced metabolic rate

- weight gain

- muscle weakness

- insomnia, anxiety

- depression

- dry cold skin

List diseases associated with GH excess pre/post puberty

Adult - acromegaly (growth of bones in skull, hands, feet and thickening of connective tissue)

Children - gigantism

What is the result of GH deficiency in embryogenesis

Dwarfism

What is cushing's syndrome (causes and symptoms)

Causes: excessive cortisol (tumour, chronic stress, drug use)

Symptoms: moon face, buffalo hump, redistribution of body mass, central adiposity, thinning of hair and skin

Primary cancers that occur in the skin and eye

melanoma, squamous cell carcinoma, basal cell carcinoma

Cutaneous melanoma vs skin carcinoma

CM: melanocyte origin, fast and spreads, severe sunburn at a young age

SC: keratinocyte origin, slow and localised, increasing age and UV exposure

Gout

Aetiology: common systemic metabolic disorder

Pathogenesis: hyperuricemia in vulnerable people, monosodium urate crystals form in joints/soft tissue, causing pain and inflammation

Joints affected: big toe, hands

Risk population: First Nations, increasing age

Rheumatoid Arthritis (RA)

Aetiology: systemic autoimmune disease causing destruction of synovial joints

Pathogenesis: joints affected by chronic inflammation, repeated attempts at repair, irreversible destruction, joint function loss and deformities

Joints affected: small joints

Risk population: women

Osteoarthritis (OA)

Aetiology: wear and tear resulting in loss of cartilage

Pathogenesis: little inflammation causes reactive bone growth and swelling in surrounding soft tissue, causing pain

Joints affected: weight bearing joints

Risk population: elderly, overweight, high exercise

Open Fracture

compound - breaks skin barrier

Closed Fracture

simple - clean break

comminuted - multiple pieces

greenstick - not a full fracture

pathologic - bone already weakened by disease

How may healing of fractures be impaired

movement, infection, misalignment

Factors that contribute to attaining peak bone mass

genetics, nutrition, physical activity, hormonal stimuli

Osteoporosis

Risk factors: ageing, sarcopenia, amenorrhea, cushing's disease, hyperthyroidism, smoking, low initial bone mass

Consequences: increased chance of fractures

Accelerated: NSAIDs, oestrogen blockers, corticosteroids

Slowed: hormone replacement at menopause, vitamin D, protein, calcium

Tumours in the Skeletal System

Chondrosarcoma, osteosarcoma

Why are the bones frequently affected by metastatic cancer

- good site for tumour cells to become trapped

- large arterial blood supply

What impact does renal failure have on the muscuskeletal system

loss of kidney response to PTH --> no VD activation --> decreases Ca absorption by blood, Ca lost in urine --> break down bones to release Ca --> renal osteodystrophy + soft tissue calcification

Main Tumours in Reproductive Systems (Testes)

(Malignant)

Origin: germ cell

Nomenclature: teratoma, seminoma

Main Tumours in Reproductive Systems (Prostate)

(Malignant/benign)

Origin: glandular epithelium

Nomenclature: adenocarcinoma, adenoma

Main Tumours in Reproductive Systems (Penis)

(Malignant/benign)

Origin: stratified squamous epithelium

Nomenclature: SCC, papilloma

Main Tumours in Reproductive Systems (Vulva)

(Malignant/benign)

Origin: stratified squamous epithelium

Nomenclature: SCC, papilloma

Main Tumours in Reproductive Systems (Ectocervix)

(Malignant/benign)

Origin: stratified squamous epithelium

Nomenclature: SCC, papilloma

Main Tumours in Reproductive Systems (Endocervix)

(Malignant/benign)

Origin: simple glandular epithelium

Nomenclature: adenocarcinoma, adenoma

Main Tumours in Reproductive Systems (Uterus - myometrium)

(Malignant/benign)

Origin: smooth muscle cells

Nomenclature: leiomyosarcoma, leiomyoma

Main Tumours in Reproductive Systems (Uterus - endometrium)

(Malignant/benign)

Origin: glandular epithelium

Nomenclature: adenocarcinoma, adenoma

Main Tumours in Reproductive Systems (Fallopian tubes)

(Malignant/benign)

Origin: glandular epithelium

Nomenclature: adenocarcinoma, adenoma

Main Tumours in Reproductive Systems (Ovary)

- Germ cell (B): teratoma

- Benign epithelial tumour cell within teratoma (M): teratocarcinoma

- Glandular epithelium (M/B): cystadenocarcinoma, cystadenoma

Main Tumours in Reproductive Systems (Breast)

(Malignant/benign)

Origin: glandular epithelium

Nomenclature: adenocarcinoma, fibroadenoma

Pelvic Inflammatory Disease (PID) Causes and Consequences

Cause: untreated gonorrhoea/chlamydia (ascending infection)

Consequences: ectopic pregnancy, infertility, pain, spread of infection into peritoneum and blood

Consequences of Endometriosis

- pain

- scarring

- adhesions impacting other organs

- ectopic pregnancy and infertility

Complications of Cryptorchidism (undescended testes)

- risk of cancer

- risk of trauma

- not functional unless surgically fixed

Examples of Teratogens

- prescription drugs

- smoking

- alcohol

- chemotherapy

- radiation therapy

- rubella

- zika

- syphillis

Why do we test for STIs in pregnancy

- some STIs are teratogenic (syphilis)

- some STIs cause damage to eyes/lungs (gonorrhoea/chlamydia)

Endocrine and Reproductive Disorders that Increase the Risk of Type II Diabetes

- Gestational diabetes

- PCOS

- Cushing's syndrome

- Acromegaly

- Truncal obesity

Explain the main acute and chronic conditions that atherosclerosis of the carotid and cerebral arteries can cause

Chronic: accelerates atrophy of the brain, loss of functional tissue in the brain leading to vascular dementia, subdural hematomas

Acute: risk of thrombus which can occlude blood vessels or thrombus turns to embolism = ischemic stroke (necrosis), aneurysm (SOL) rupturing = haemorrhagic stroke = herniation/death

Epidural Haematoma

Aetiology: rupture of the dural arteries following trauma

Pathogenesis: blood accumulates rapidly between skull and the dura mater due to high arterial pressure

Outcomes: increased intracranial pressure, brain herniation, death (rapid surgical intervention)

Subdural Haematoma

Aetiology: tearing of bridging veins located between dura and arachnoid

Pathogenesis: displacement of skull causes brain to move within the CSF, stretching/tearing bridging veins

Outcomes: self-limiting, increased intracranial pressure, brain herniation, death

Subarachnoid Haematoma

Aetiology: trauma resulting in an arterial haemorrhage from a congenital aneurysm

Pathogenesis: arterial bleed result in rapidly accumulating haematoma

Outcomes: increased intracranial pressure

What determines whether a SOL causes atrophy or herniation

Slow = atrophy

Fast = herniation

SOL (space occupying lesion) Examples

Tumours, haematomas, oedema/swelling, abscess, hydrocephalus, aneurysm

How do microbes enter the CNS

- direct implantation (surgery/trauma)

- blood

- extension from local site (tooth/sinuses/eyes/ears)

- PNS

CSF Appearance of Pyogenic Meningitis vs Viral Meningitis

Viral: normal glucose, lymphocytes, slight increase in proteins

Pyogenic: cloudy, increased proteins, reduced/absent glucose, neutrophils

Age-related Diseases in CNS

- cerebrovascular disease

- stroke

- alzheimer's

- parkinson's

- glioblastoma

- carcinoma

What is required for the digestion, absorption and metabolism of nutrients

Metabolism - liver

Digestion - pancreatic enzymes

Absorption - pancreatic + brush border enzymes (proteins/carbohydrates), bile (fat), large surface area

How does malabsorption happen

Site of absorption is compromised

- reduction of small intestine surface area (crohn's, ulcers, cancer)

- obstruction to bile (liver failure, stones, tumours)

- obstruction of pancreas (chronic pancreatitis, stones, tumours)

Risk factors for the development of cancers of the tube and accessory organs

Oral-pharyngeal: ageing, alcohol, smoking, HPV

Upper oesophagus: ageing, alcohol, smoking, HPV

Lower oesophagus: chronic gastric reflux

Stomach: chronic gastritis, ulcers, pylori infection, NSAIDs, alcohol, smoking, ageing

Colon: ageing, genetics, smoking, alcohol, IBS, visceral obesity, low fibre, high saturated fat, refined carbohydrates, processed meats, genetics

Consequences of Chronic IBS

- cancer

- scarring = adhesions, fistula formation, obstruction

- chronic blood loss = anaemia

- malabsorption

- pain

- bloody diarrhoea

Risk factors for gallstones

- fat

- female

- fertile

- forties

-family history

Consequences of gallstones

- pain

- acute/chronic cholecystitis

- chronic inflammation

- cancer

- obstruction = cholestasis and cirrhosis

- pancreatitis

- jaundice

- malabsorption

Main causes of cirrhosis (chronic inflammation of the liver)

- chronic alcohol intake

- hepatitis

- autoimmune disease

- iron overload

- biliary disease

- heart failure

Life-threatening conditions from cirrhosis before liver failure

1. increases risk of hepatocellular carcinoma

2. scarring leading to compression and obstruction of veins in the liver = portal hypertension = chance of vein rupture

3. encephalopathy due to increased ammonia = disruption of CNS/coma/death

How liver failure can worsen conditions caused by cirrhosis

1. portal hypertension = congestion = increased hydrostatic pressure = oedema + ascites: liver failure reduces synthesise of plasma proteins leading to reduced colloidal pressure, worsening oedema + ascites

2. portal hypertension = congested veins = prone to rupture/hemorrhage: liver failure means no clotting factors are being produced leading to being more prone to spontaneous haemorrhage

Effects liver failure has on the body

- malabsorption of vitamins (A,D,E,K)

- weight loss

- chronic posioning

- jaundice

- oestrogenaemia

- hyperaldosteronism

- encephalopathy