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2023 > 520 learning objectives > Flashcards

520 learning objectives Flashcards

1
Q

Define Hyperaemia

A

Increase in blood flow

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2
Q

Define Oedma

A

Increase in interstitial fluid - swelling

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3
Q

Define Effusion

A

Oedema in body cavity

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4
Q

Define Resolution

A

Healing without scar tissue

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5
Q

Define Organisation

A

Healing with scar tissue

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6
Q

Define Exudate

A

Extravascular fluid low high in protein concentration

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7
Q

Define Transudate

A

Extravascular fluid with low protein concentration

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8
Q

What form of cell death causes an inflammatory response

A

Necrosis - passive process of cell death which kills surrounding cells (infarct)

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9
Q

What are the 3 features of acute inflammation?

A
  1. Hyperaemia - dilation and increase in blood flow
  2. Oedema - increase in interstitial fluid
  3. Neutrophils - Leukocytes
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10
Q

3 possible outcomes of acute inflammation

A
  1. Healing by Resolution - without scar tissue
  2. Healing by Organisation - healing with scar tissue
  3. Chronic inflammation
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11
Q

3 components of granulation tissue and their role/purpose

A

Macrophages - role to phagocytose debris, pathogens and neutrophils while producing chemical mediators to recruit Fiberblasts.
Fiberblasts - synthesise collagen fibers
angiogenesis - forms new blood cells.

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12
Q

Consequences of healing by organisation?

A
  • healing by scar tissue
  • loss of function
  • replacing normal functioning tissue with tissue that is just filling the gap.
  • weakens walls of the vessel which increases risk of atheroscleorsis and aneurysm
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13
Q

3 causes of chronic inflammation?

A
  1. repeated acute inflammation
  2. repeated stimulus
  3. special cases
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14
Q

3 features of chronic inflammation

A
  1. healing by organisation
  2. granulation tissue
  3. lymphocytes
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15
Q

Negative outcomes of chronic inflammation

A
  • scarring
  • loss of functional tissue
    -weakens walls of the vessel which increases risk of atherosclerosis and aneurysm
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16
Q

Define Ischaemia

A

Lack of blood supply

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17
Q

Define thrombus

A

Blood clot attached to the wall of an artery , vein or ventricle of the heart.

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18
Q

Define Embolus

A

Any blood clot or substance that is undissolved in the blood, flowing through a vessel until it become too small to pass through, causes an occlusion and restrictive blood flow.

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19
Q

Define Aneurysm

A

Excessive localised dilation of the wall of an artery, if burst can cause haemorrhage.

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20
Q

Atherosclerosis

A

Chronic inflammation of the wall of an artery. Thickening of the wall due to a build up of plaque, causes restricted blood flow.

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21
Q

Define Stasis

A

Blood that is not moving. Shouldn’t affect high pressure sites like arteries but effects low pressure sites like veins.

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22
Q

Identify blood flow & pressure differences in the systemic, pulmonary & (systemic) venous circuits:

A

Systemic circulation carries oxygenated blood from the left ventricle, through the arteries, to the capillaries in the tissues of the body. From the tissue capillaries, the deoxygenated blood returns through a system of veins to the right atrium of the heart.

The pulmonary circulation is a high flow, low resistance pathway. Blood flows through the tricuspid valve into the right ventricle. It then flows through the pulmonic valve into the pulmonary artery before being delivered to the lungs.

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23
Q

Superficial vs Deep vein thrombi

A

Superficial vein thrombosis refers to a blood clot close to the surface of the skin, rarely embolise, but do cause pain.
Deep vein thrombosis is a blood clot deep in the veins, they often embolise and are asymptomatic.

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24
Q

How do the kidneys contribute to systemic hypertension?

A

Kidney plays increase blood pressure via extracellular fluid volume regulation acquired through salt reabsorption activity, under the control of the renin–angiotensin–aldosterone system (RAAS).

RAAS is activated when there is a drop in blood pressure (reduced blood volume) to increase water and electrolyte reabsorption in the kidney; which compensates for the drop in blood volume, thus increasing blood pressure.

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25
Q

What does Atherosclerosis predispose?

A

Atherosclerosis predisposes the risk of myocardial infarction, stroke and vascular diseases. It also predisposes the risk of aneurysm in the area of atherosclerosis as the wall of the vessel becomes weakened.

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26
Q

What is the difference between angina and myocardial infarction?

A

A myocardial infarction is a loss of blood supply to the heart caused by a complete occlusion of an artery which causes death by necrosis.

Angina is a transient loss of blood supply, meaning blood returns before the cells die by necrosis. Can be treated with vasodilators or a splint.

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27
Q

Describe the inflammation and repair that occurs following a MYocardial Infarction

A

A myocardial infarction is death of cells by necrosis in the myocardium which results in acute inflammation - hyperaemia, oedema, neutrophils.

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28
Q

Complications that can occur following a MI.

A

Following a myocardial infarction, normal functioning tissue is replaced with scar tissue which has no electrical functions. This can cause arrhythmia’s. The scar tissue is weaker which makes the heart weaker and can lead to heart failure.

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29
Q

Causes of Left vs Right sided heart failure.

A

Ride side received oxygen poor blood from veins and pumps it to the lungs, where the blood picks up oxygen and gets rid of carbon dioxide.
The left side of your heart receives oxygen-rich blood from your lungs and pumps it through your arteries to the rest of your body.

In left-sided heart failure, the left side of the heart is weakened and results in reduced ability for the heart to pump blood into the body. More prone to heart failure.

In right-sided heart failure, the right side of the heart is weakened and results in fluid in your veins, causing swelling in the legs, ankles, and liver.

30
Q

Backward effects of left vs right sided heart failure

A

Right sided - Pulmonary congestion leading to pulmonary oedema

31
Q

Forward effects of HF - compensatory mechanisms etc.

A

The kidneys activating RAAS as a result of reduction in cardiac output.

32
Q

Common causes of pericarditis

A

Inflammation around the myocardial sac. Can be caused by bacteria, infection.

33
Q

Common causes of endocarditis

A

Inflammation in the inner lining of the heart, including valves. Caused by unresolved acute inflammation, special cases. Bacterial endocarditis - bacteria in a sterile site.

34
Q

What effects can endocarditis have?

A

Valves lose the ability to open and close. Bacterial endocarditis thrombus can turn into emboli and spread bacteria to different organs.

35
Q

Role of Angiotensin 2 in RAAS

A

Angiotensin 2 causes the muscular walls of arterioles to constrict which increase blood pressure. This triggers the adrenal glands to release aldosterone which is useful in retention of sodium and water intake.

36
Q

Role of Aldosterone

A

Aldosterone causes the kidneys to excrete potassium through the urine. The increase in sodium in the bloodstream causes retention of water, increasing blood volume and blood pressure.

37
Q

EXPLAIN THE IMPACT THAT RENAL FAILURE HAS ON THE REST OF THE BODY

A

a) Over-activation of RAAS leading to the retention of sodium & water thus increasing blood volume as well as vasoconstriction of arteries & arterioles thus causing increased resistance; together this leads to hypertension (which can cause atherosclerosis, left- ventricular hypertrophy & failure) & increased hydrostatic pressure causing oedema (oedema is worsened if there is also proteinuria causing reduced colloidal osmotic pressure.

b) Decreased erythropoietin (EPO) - red blood cell producer - leads to anaemia. possibe hypoxia. Heart rate increases

c) Reduced activation of vitamin D & increased urinary loss of calcium & serum retention of phosphate causes hyperparathyroidism which leads to renal osteodystrophy & soft tissue calcification.

d) Acidosis leading to hyperkalemia, which can cause cardiac arrhythmias.

e) Increased wastes within the blood leading to lethargy & nausea.

f) Loss of bone mass coupled with lethargy leads to muscle atrophy.

38
Q

WHAT ARE THE MAIN MALIGNANCIES THAT AFFECT THE MALE & FEMALE URINARY SYSTEMS?

A
  1. Prostate: Adenocarcinoma (increased incidence with age)
  2. Nephroblastoma (rare childhood carcinoma)
  3. Renal cell carcinoma
  4. Transitional carcinoma
39
Q

WHAT ARE COMMON CAUSES OF GLOMERULONEPHRITIS & POSSIBLE CONSEQUENCES?

A

Acute Kidney Failure: Inflammation and damage to filtering part of kidneys - glomerulus. Toxins, metabolic waste and excess fluid not properly filtered to urine.

Causes:
- swelling of endothelium
- decreased BF
- Inflammation altering permeability

Results in:
- Rapid over-activation of RAAS
- Decreased urinary output
- proteinurea - protein in urine
- Haematuria - Blood in urine.

40
Q

WHY IS THE RENAL PAPILLA SUSCEPTIBLE TO TOXIC INJURY & ASCENDING INFECTIONS?

A

Nipple like structure.
Area of the kidney where urine is at its most concentrated > can be affected by toxic injury > first bit of the kidney proper where an ascending infection will get to.

41
Q

WHAT ARE THE MAJOR DIFFERENCES BETWEEN ASCENDING & DESCENDING INFECTIONS & WHY ARE THE FORMER MORE COMMON IN FEMALES VERSUS MALES?

A

Ascending: up through GI Tract
Women are more prone to UTIS as the urethra is shorter than that of males.

Descending infections effect male and females equally. Down through the blood, will knock out both kidneys.

42
Q

Possible Consequences of Urinary Stones

A

Caliculi – Stones
Consequences of caliculi:
- One stone predisposes to further stones.
- Predisposes to stasis urine.
- Mucoproteins
- pH
- infection
- dehydration
- calcium metabolism disorders.
- Haemorrhaging
- Blood in urine as underlying epithelium can be damaged.
- Hydronephrosis – urine backing up into kidney.
- Increased risk of cancer.

43
Q

**Which is more likely to result in renal failure:
a. Ascending infections
b. Descending infections

A

b as it is more likely to affect both kidneys

Descending infections are more serious as they are blood born so will lead to damage of both kidneys & potentially all nephrons and thus can cause renal failure. An infection in the blood can also lead to meningitis, encephalitis & osteomyelitis all of which we will cover in future weeks.

Ascending infections are from the lower urinary tract & may only damage one kidney or part of one kidney.

44
Q

Osteoarthritis

A

Wear and Tear resulting in loss of cartilage.

Little inflammation compared to other forms of arthritis but reactive bone growth and swelling surrounding soft tissue causes pain.

Tends to affect weight bearing joints.

As it is wear and tear, commonly in elderly, athletes – runners, afl, netball.

45
Q

Rheumatoid Arthritis

A

Autoimmune destruction of joints that may affect any synovial joint in the body and causes systemic inflammation.

Affects women more than men.

Can be diagnosed at any age but typically first diagnosed middle age.

Joints are affected by chronic inflammation (type IV cell mediated response); formation of pannus, bone erosion, cartilage and tendon degradation -> irreversible joint deformation.

46
Q

Gout

A

Common Systemic Metabolic disorder

Hyperuricaemia in vulnerable people – not everyone with hyperuricaemia gets gout.

Monosodium urate crystals form in joints and soft tissues causing severe pain & inflammation.

Increased incidence with age.

Often affects male’s big toe. Rare in women before menopause. After menopause commonly affects hands.

47
Q

List the factors that contribute to attaining peak bone mass.

A

Genetics, nutrition, exercise, weight bearing activity.

48
Q

List the risk factors for the development of osteoporosis; the possible consequences of osteoporosis & how bone loss may be retarded/accelerated.

A

Factors include ageing, reduced weight-bearing physical activity, sarcopenia, amenorrhea, loss of oestrogenic activity after menopause and low initial bone mass.

To prevent osteoporosis, it is important to get out pear bone mass which is determined by genetics, nutrition and physical activity while growing up to our early 20s.

49
Q

List the tumours that occur in the skeletal system (reviewing what was covered in neoplasia week).

A

Osteosarcoma – malignant bone tumour
Chondrosarcoma – malignant cartilage tumour

50
Q

Why are the bones frequently affected by metastatic cancer?

A

Bone is very vascular, so arterial metastases are easily distributed to this site. Bone metastases are found in more than 25% of people who die from cancer overall, but 75% of people who die from breast cancer.

51
Q

What impact does renal failure have on the musculoskeletal system?

A

When in renal failure, the kidneys stop activating vitamin d, without vitamin d production, dietary calcium is not absorbed.

Healthy kidneys activate vitamin D which is required by the gut to absorb calcium and the kidneys regulate the levels of calcium and phosphate in the blood. Under the influence of parathyroid hormone (PTH) the healthy kidneys activate more vitamin D, secrete phosphate, and reabsorb calcium from the filtrate thus keeping it in the blood.

Chronic renal failure can cause renal osteodystrophy – under mineralisation of bone and soft tissue calcification. In failure, the kidney may not be able to convert vitamin D into its active metabolite and without vitamin D the gut cannot absorb calcium from food, which results n low levels of serum/blood calcium.

52
Q

Type 1 Diabetes - Compare & contrast type I & II diabetes inc causes, pathogenesis, typical initial clinical presentation (prior to diagnosis/treatment) & possible consequences.

A

Aetiology - Autoimmune loss of pancreatic beta cells from the immune attack means can’t make insulin.

Pathogenesis - Without insulin, target tissue starves. Fat, muscle, liver need insulin.

Initial presentation - Present as acute medical emergency. Altered level consciousness etc.

Consequences -
All Fuel sources cause acidosis.
Lose blood volume because peeing so much. Constantly hungry as target tissues are starving. Altered consciousness.

53
Q

Type 2 Diabetes - Compare & contrast type I & II diabetes inc causes, pathogenesis, typical initial clinical presentation (prior to diagnosis/treatment) & possible consequences.

A

Lifestyle
Aetiology - Strong genetic predisposition, environment, and lifestyle factors. Key issue is insulin insensitivity or resistance

Pathogenesis -
The person makes insulin but target tissue don’t respond to insulin as they should.
Target tissues take up enough blood glucose to keep themselves happy but not enough to reduce BGL to normal. Hypoglycaemia.

Initial Presentation - Reversible if weight is lost. Otherwise progresses to point were beta cells burn out and is then irreversible

Consequences -
Neuropathies – nerve damage
Nephropathy – kidney damage
Cardiovascular disease
Cerbrodiseases
Peripherovasculardisease
Eye diseases

54
Q

Understand what is meant by ‘functional’ tumour & the possible implications for hormone levels.

A

Functional tumours make too much of a certain hormone and cause symptoms.

Non-functional tumours may make hormones but don’t cause any symptoms.

Functional tumour means well differentiated, still making hormone, see an excess amount of that hormone. If not, functional we lose the ability to make that hormone.

55
Q

What is the most common cause of hyperthyroidism & the symptoms associated with the condition?

A

Hyperthyroidism happens when the thyroid gland makes too much thyroid hormone.

Hyperthyroidism speeds up the body’s metabolism.

That can cause many symptoms, such as weight loss, hand tremors, and rapid or irregular heartbeat.

56
Q

How does GH excess differ in pre/post puberty?

A

In adults, GH excess results in acromegaly – excessive growth of bones in the skull, hands and feet and a thickening of connective tissue leading to coarsening of appearance.

In children the growth plates have yet to fuse, so gigantism is experienced.

57
Q

Result of GH deficiency in embriogenesis

A

Results in dwarfism

58
Q

What is Cushing’s syndrome & how may it be caused?

A

When the body makes too much of the stress hormone, cortisol over a long period of time.

Excessive cortisol or use of corticosteroids. The hormone regulates blood pressure and blood glucose levels and the lack of this results in depression, anxiety, and irritability from excessive stress.

Can cause increased fat depositions in the trunk and face, development of buffalo hump, muscle atrophy weakness, osteoporosis.

59
Q

Primary cancers of skin and eye

A

Melanoma, BCC, SCC

Melanoma:
-Requires fewer mutations to get an aggressive melanoma versus carcinoma and these cancers are not strongly associated with increased age.

-Increased risk is not associated with a dose dependent exposure to UV but rather a severe sunburn a young age.

-Some people are genetically predisposed, others with increased risk include fair skinned, blue green eyes.

-Tend to grow vertically rather than radially so unlike SCC/BCC they have often metastasized at time of diagnosis.

Basal Cell Carcinoma BCC:
-Most common carcinoma
-Increases in incidence with age and exposure to UV, sun, radiation.
-Tend to grow very slowly due to high rate of apoptosis and radially as a papule.
-Rarely metastasize.

Squamous cell carcinoma SCC:
-Very common carcinoma
-Increases with incidence with age, UV exposure, radiation, sun exposure.
-Tends to grow more slowly than melanoma but faster than BCC.
-Usually diagnosed prior to metastasis in Australia.

60
Q

List the main types of fractures & how healing may be impaired.

A

Green stick, simple, compound, comminated, spiral, haematoma, soft callous, hard callous, remodelling.

Systemic inflammatory conditions such as arthritis, diabetes mellitus, sepsis or multiple trauma affect the fracture healing and impairment time.

61
Q

List the main causes & potential consequences of pelvic inflammatory disease (PID).

A

Gonorrhoea and Chlamydia.

If not removed, is a leading cause of ectopic pregnancy due to scarring and adhesions. Adhesions may form between the GIT, urinary and reproductive systems causing possible obstructions and fistula formation.

Inflammation may result in walling off of the infected ovaries in an attempt to contain the infection thus forming absences, if they structures rupture the result is peritonitis, which can be fatal. If the infection gets into the blood can cause sepsis.

PID causes scarring in the fallopian tubes which can inhibit the transmission of sperm/ova. Sperm are a smaller cell type compared to ova and developing zygote so sperm may pass through a constricted tube but the ova and zygote are too large so the sperm implants in the fallopian tube wall.

62
Q

List the possible consequences of endometriosis?

A

Endometriosis causes inflammation and healing by organisation.

The scar tissue can cause obstruction to the fallopian tubes, bowel and bladder. Pain

63
Q

What are the possible complications of cryptorchidism?

A

Undescended teste can cause trauma, cancer, infertility.

Absences of at least one of the testicle from the scrotum.

64
Q

List some examples of teratogens, why do we test for STIs in pregnancy.

A

Infections like Zika, Rubella, Syphilis. Drugs, Alcohol and irradiation, maternal transmission of chlamydia or gonorrhoea can cause conjunctival scarring of the new born eyes but is not strictly a teratogenic.

65
Q

List some of the endocrine conditions that increase the risk of developing diabetes type 2

A

Gestational diabetes because pregnancy is naturally diabetogenic state. Polycystic ovarian syndrome (PCOS), Cushing’s syndrome, acromegaly, and truncal obesity.

66
Q

List the 4 main COPDs (asthma, chronic bronchitis, bronchiectasis & emphysema), their causes & possible consequences, pay particular attention to atopic asthma.

A
  1. Chronic bronchitis
    A persistent cough that lasts for at least 3 months over at least 2 years. Permanent changes in airway. Risk of obstruction.
    Increase of smooth muscle, thickening of bronchial walls which causes a resistance of airflow.
  2. Emphysema
    Irreversible and progressive destruction of alveolar walls without obvious fibrosis.
    Causes abnormally large airspaces. Inflammation and loss of elasticity.
  3. Bronchiectasis
    Irreversible and progressive dilation of bronchi and bronchioles. Causes destruction of elastic and muscle. Chronic nectrotising infection of the bronchi and bronchioles.
  4. Bronchial Asthma
    Hyper reactive airways.
67
Q

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

A

Chronic restrictive disease. Inhaled stimuli causing inflammation. Scarring within the lungs. Risk of heart/lung failure and

68
Q

Why are the lungs a common site for secondary cancers?

A

All venous blood goes back to lungs for oxygenation.

69
Q

How are the lungs affected by left ventricular failure?

A

Pulmonary Oedema

70
Q

How do lung diseases contribute to right ventricular failure?

A

Lung diseases alter perfusion/ ventilation and cause normally low pressure pulmonary circuit to be high pressure circuit.

71
Q

What determines whether a SOL causes atrophy or herniation, give some examples?

A

2023 (4 decks)

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