1
Q
Outline the mechanisms for maintaining acid / base (pH) homeostasis
A
- Acid-base balance is achieved through regulating the excretion (output) of acids and/or bases as necessary (e.g. lungs can excrete or conserve acids via ventilation, kidneys can excrete or conserve acids or bases in urine)
- Until this occurs, buffering is a temporary solution to reducing changes in blood pH (7.35-7.45)
2
Q
Describe each of the following pH imbalances and list common causes and compensatory mechanisms for each: Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis
A
- Respiratory acidosis: decr. release CO2 –> excess H+ in the blood –> fall in blood pH. Caused by: Depression of brainstem respiratory centers or failure of ventilation by i) decr. neuromuscular control of ventilation or ii) respiratory conditions/hypoventilation/decreased gas exchange (e.g. increased airway resistance, COPD, pneumonia). Renal mechanisms compensate through incr. retention of bicarbonate (HCO3-) and excretion of acids (H+).
- Respiratory alkalosis: excess release CO2 –> lack of blood H+ –> rise in pH. Caused by hyperventilation due to hypoxemia, pain, anxiety/fear, fever or sepsis. Renal mechanisms compensate through increased secretion of bicarbonate (HCO3-) and increased retention of acids (H+).
- Metabolic acidosis: Too much bicarbonate (HCO3-) is excreted/lost or if there is an increase in acid production/exposure, then blood pH will fall. Occurs due to increased bicarbonate loss (normal anion gap metabolic acidosis) via renal loss (i.e. with renal failure) or GI loss (e.g. diarrhea, pancreatitis) OR increased acid production/exposure via increased lactic acid production (e.g. increased anaerobic respiration due to ischemia or hypoxemia), ketoacidosis (alcoholic, diabetic, starvation), exposure to certain toxic substances (e.g. anti-freeze, glues), or certain medications (e.g. paracetemol, aspirin). Respiratory mechanisms attempt to compensate via hyperventilation.
- Metabolic alkalosis: Too much hydrogen/acids lost or too much bicarbonate retained –> rise in blood pH. Occurs due to: increased acid loss (increased renal loss (e.g. diuretics, increased liquorice ingestion, Cushing’s syndrome), GI loss (e.g. vomiting)), increased bicarbonate retention (excess administration of bicarbonate (i.e. IV saline solution)) or dehydration (which can result in both acid loss and bicarbonate retention). Respiratory mechanisms attempt to compensate via hypoventilation.
3
Q
Outline the causes and implications of each of the following electrolyte imbalances: Hyponatremia Hypernatremia Hypokalemia Hyperkalemia
A
- Hypernatremia: Increased sodium levels in the blood. Caused by either sodium gain or water loss in the ECF. Increased ECF osmolarity –> water leaves cells and shrink –> cellular dysfunction. (Also Cl- follows Na+ causing hyperchloremia)
- Hyponatremia: Decr. sodium levels in the blood. Caused by either sodium loss or water gain in the ECF. Decr. ECF osmolarity –> water enters cells –> swelling –> cellular dysfunction. (Cl- follows Na+ causing hypochloremia).
- Hyperkalemia: Incr. in potassium levels in the blood (rare) caused by: Increased intake (rarely dietary), shift from ICF to ECF (can occur as a result of cell damage), decreased renal excretion.
- Hypokalemia: Too little potassium (K+) in the blood. Caused by reduced dietary intake, increased entry of K+ into cells, increased loss of K+ from body/increased renal secretion
4
Q
Describe the 4 buffering systems (for acids)
A
- Bicarbonate buffer system: most important buffering system of the ECF. Begins with the movement of CO2 into the blood from body tissues, which reacts with water to form carbonic acid (H2CO3), which readily dissociates into a hydrogen ion (H+) and a bicarbonate ion (HCO3-). The bicarbonate ions make up the bicarbonate buffer system which is an alkaline reserve that is available to pick up excess H+. This system buffers most of the metabolic acids produced by cellular respiration.
- Protein buffer system: proteins in either plasma (mainly albumin) or within ICF (e.g. amino acids) which can bind H+ ions.
- Haemoglobin buffer system: haemoglobin (Hb) in red blood cells can buffer the H+ generated by the above (carbonic acid) reaction. Hb buffering of H+ also facilitates the offloading of O2 at body tissues.
- Phosphate buffer system: mostly buffers acids within urine, but is also an important buffer in the intracellular fluid (ICF) (and can also buffer in the ECF).
5
Q
Describe the pathophysiology of urinary tract obstruction
A
- The obstruction may be anatomical or functional
- Obstruction of the renal tract results in dilation of the parts of the tract proximal to the obstruction and the accumulation of urine- hydroureter and/or hydronephrosis. Progressively, this backup of urine flow affects first the distal nephrons, then proximal nephrons and eventually the glomeruli, causing damage and reduction in kidney tissue
6
Q
Outline the effects and pathophysiology of infections of the urinary tract
A
- inflammation of the urinary tract by microorganisms
- Cystitis: inflammation of the bladder due to ascending microbes (via urethra). Can lead to pyelonephritis.
- Pyelonephritis: inflammation of the renal pelvis and interstitium due to ascending microbes or microbes in blood
7
Q
Describe acute kidney injury (AKI), including its causes, pathophysiology & management
A
- sudden decline in renal function resulting in a decreased ability of the kidneys to regulate fluid, electrolyte and acid-base balance
- Causes:
1. Prerenal: relate to impairments in renal blood flow
2. Intrarenal (intrinsic): due to abnormalities or complications within the kidney(s) itself
3. Postrenal: relate to complications within the renal tract that affect kidney function - Patho: Acute renal injury is associated with a reduction of GFR by 25% or more, oliguria (in most cases) and retention of metabolic wastes, particularly azotemia; these changes typically occur within a few hours to days of the initial insult.
- Treatment: Management is related to the identification and treatment of underlying causes and also includes maintenance of adequate fluid, electrolyte and acid-base balances adequate nutrient intake prevention/management of infection
8
Q
Outline the pathophysiology of two of the major intrinsic causes of AKI- glomerulonephritis and actue tubular necrosis
A
- Glomerulonephritis (Inflammation of the glomerulus): disruption of the filtration membrane that usually results in inadequate GFR, but also increased glomerular permeability.
- Actue tubular necrosis: tubular epithelial cells of the nephron are damaged due to ischemia and/or nephrotoxins. As the cells of the tubule die, they slough off and plug up the nephron, resulting in a back-up of filtrate and increased capsular hydrostatic pressure
9
Q
Describe chronic renal disease, including its causes, pathophysiology & management
A
- Progressive and irreversible destruction of nephrons. There is a progressive reduction in GFR and subsequent reductions in nephron function and other kidney functions.
- Most common causes: diabetes mellitus, hypertension, glomerulonephritis, polycystic kidney disease
- Nephrons that are still functioning adapt to pick-up the extra ‘workload’ and the kidneys continue to excrete relatively normal levels of water and solutes. However, this eventually results in these nephrons succumbing to dysfunction and nephron loss continues to progress. End-stage kidney disease occurs when there is less than 10% of renal function remaining.
- Management: depends on the stage of the disease. Generally in the early stages management is around trying to slow progression of the disease (e.g. dietary control with adequate calorie intake and: protein restriction, Vit D supplementation, fluid evaluation, sodium, potassium & phosphate restriction, hyperglycemic control & insulin (for patients with diabetes), etc.). End-stage requires dialysis or renal transplant for survival.
10
Q
Define shock and distinguish between the different types of shock
A
- Shock occurs when the cardiovascular system fails to maintain adequate tissue perfusion, resulting in widespread impairment of cellular metabolism and function.
- Neurogenic, cardiogenic, septic, anaphylactic, hypovolaemic, obstructive.
11
Q
Outline the pathophysiology of impaired cellular metabolism as a result of decreased tissue perfusion
A
- Adequate tissue perfusion is essential to ensuring gas, nutrient and waste exchange can occur in body tissues to sustain normal cellular metabolism
- Therefore inadequate perfusion prevents normal cell metabolism which causes cellular dysfunction leading to tissue/organ failure
- E.g. decr. cellular oxygen (–> anaerobic resp) and decr. cellular glucose (–> alters glucose metabolism)
12
Q
Compare the causes and pathophysiology, including signs & symptoms, of the different types of shock
A
- Neurogenic; widespread vasodilation bc incr. PNS + decr. SNS. Causes incl. medulla/sprinal cord injury, decr. O2/glucose to medulla, depressive drugs, anaesthetic agents, severe emotional stress/pain. Signs: hypotension and bradycardia
- Septic; infectious microorganisms in bood (causing systematic inflammatory response which affects tissue perfusion). Signs incl. temp instability, tachycardia, incr. RR, hypoxemia, incr. WBCs, oliguria, confusion
- Cardiogenic; decr. CO (despite normal vol) leading to tissue hypoxia. Caused by anything that decr. CO (e.g. MI), signs incl. pulmonary oedema, hypotension, oliguria, SOB, nausea/vom
- Anaphylactic; hypersensitive allergic reaction, leading to widespread vasodilation and peripheral pooling. Signs incl. airway constriction/resp difficulty, peripheral oedema, swelling of mouth/throat, burning sensation of skin, headache/LOC, anxiety.
- Hypovolemic; decr. blood vol. bc sig. fluid loss. Caused by hemorrhage, plasma loss (burns), dehydration, diabetes, diuresis, vom/diarrhoea.
- Obstructive; decr. CO due to obstruction/restriction of blood flow thr’ heart vessels. Caused by sig. pulmonary embolism, pulmonary hypertension, constrictive pericarditis. Signs similar to cardiogenic shock, incl. hypotension, oliguria, impaired mental activity, cool peripheries, SOB.
13
Q
Outline the various treatment options for the different types of shock
A
- Cardiogenic: re-perfusion of the heart tissue and workload management. E.g. GTN, inotropes, thrombolytics, anti-arrhythmic drugs, fluid management, O2 therapy
- Obstructive: removal/correction of the cause to restore blood flow thr’ heart chambers
- Hypovolemic: rapid fluid resuscitation w crystalloids and necessary blood products, and identification/treatment of cause.
- Neurogenic: fluid management and use of vasopressors to stabilize BP
- Anaphylactic: emergency treatment required, incl. removing allergen, IM adrenaline, fluid management, antihistamines, corticosteroids
- Septic: antimicrobial therapy, fluid resus, inotropes, vasopressors, cardiorespiratory support (O2, ventilation)
14
Q
Distinguish between different classifications and different types of anemia
A
- Different types of anemia are classified based on the size or shape of the RBC and/or the hemoglobin content of the cells
1. RBC size (MCV): - Normocytic (normal)
- Macrocytic (large)
- Microcytic (small)
2. Hb content - Normochromic (normal amount, generally max.)
- Hypochromic (less than normal amount)
15
Q
Outline the manifestations of anemia
A
- Fatigue
- Pallor or jaundice
- Heart palpitations
- SOB
Also - GI effects (nausea, abdominal pain, anorexia, etc.)
- Neurological effects (numbness, muscle weakness, spasticity)
16
Q
Describe the causes, associated risks and pathophysiology of iron deficiency anaemia
A
- Causes: inadequate dietary intake, decr. absorption, incr. requirements, excessive iron loss
- Associated risks: incr. iron req. during periods of growth and pregnancy, incr. loss w menstruation/other blood loss, reduced access to adequate nutrition (poverty, etc.), and/or certain medical conditions that affect absorption (Coeliac, Crohn’s)
- Without adequate iron, less Hb is produced and thus RBC count reduced (bc become microcytic and hypochromatic)
17
Q
Outline the causes, additional symptoms and treatments for the macrocytic anemias
A
- Causes: folate or vitamin b12 deficiency, bc req. for DNA production in developing RBCs so deficiency leads to incomplete RBC development.
- Symptoms: stomatitis/sore red tongue/cheilosis/mouth ulcers, pallor + jaundice, numbness/weakness/unsteady gait. Pernicious (no IF) can include (slow onset) consistent infections, mood changes and general GI/cardiac/renal problems
- Treatment: folate replacement back to normal then maintaining adequate dietary intake. Pernicious is treated w replacement of vit B12 injections or oral replacement therapy.
18
Q
Describe polycythemia, including the different classifications, and outline potential complications
A
- Excessive RBCs
- Classifications:
1. Relative polycythemia, increased RBCs associated w dehydration
2. Absolute polycythemia:
A) Primary, associated w gene mutation (rare)
B) Secondary, due to increased erythropoietin (EPO) secretion - Complications: increases blood viscosity –> incr. BP and incr. risk for thromboembolism and associated complications
19
Q
Define the terms leukopenia and leukocytosis and outline causative factors for each
A
- Leukopenia: reduction in WBC numbers. Can be a specific type of WBC or multiple.
Causative factors: radiation, shock, autoimmune disease/immune deficiencies, hematological conditions (e.g. anemia, leukemia), certain chemotherapy agents/other toxic drugs, and certain infections (e.g. HIV) - Leukocytosis: increase in WBC numbers beyond the normal range. Occurs as part of the normal homeostatic response, but can also occur in response to various drugs or chemicals and pathological conditions e.g. malignant disorders/hematological conditions
Causative factors: Infections, strenuous exercise, surgery, emotional stress, trauma, pregnancy
20
Q
Differentiate between the four major types of leukaemia: ALL, AML, CLL, CML
A
Acute - rapid growth of undifferentiated blood cells (blast cells)
Chronic - slow growth of more differentiated cells
1. Acute lymphoblastic leukemia (ALL): arises from lymphoid cells
2. Chronic lymphocytic leukemia (CLL): arises from more differentiated lymphoid stem cells.
3. Acute myeloid leukemia (AML): arises from myeloid stem cells
4. Chronic myeloid leukemia (CML): arises from further differentiated myeloid cells
21
Q
Outline the pathophysiology, including signs & symptoms, of leukemia
A
- Pathophysiology: uncontrolled proliferation of malignant leucocytes (WBCs), causing an overcrowding of bone marrow and decreased production and function of normal hematopoietic cells.
1. Acute; blast cells taking up space in the bone marrow and preventing the normal development of all types of blood cells, resulting in cytopenia. Eventually the malignant blast cells spill out into circulation and may then spread to other organs and tissues in the body.
2. Chronic; premature lymphocytes accumulate in the bone marrow, ultimately has the same effect as acute - cytopenia. - Signs and symptoms: same for both, but acute is rapid onset and chronic is slow.
1. fatigue (bc anemia)
2. easier bleeding
3. incr. infections
4. Pain and tenderness in the bones
5. abdominal fullness
6. Pain in the lymph nodes
22
Q
Differentiation between Hodgkin and Non-Hodgkin lymphoma
A
- Non-Hodgkin: tumour cells spread sporadically to other lymphoid tissues and organs; sub-types may be aggressive or indolent. Commonly occurs in middle age, risk factors incl. history, irradiation, certain toxins/chemicals, HIV, helicobacter pylori infection
- Hodgkin: progression from one group of lymph nodes to another and the presence of Reed-Sternberg (RS) cells.
2 types, classical and nodular lymphocyte predominant. Tends to affect young or more elderly adults. Risk factors incl. HIV infection and previous infections w Epstein-Barr virus.
23
Q
Outline the pathophysiolgy, including signs & symptoms, of lymphoma
A
- Pathoohysiology: genetic abnormalities develop within lymphocytes which result in uncontrolled proliferation of malignant cells. The growing neoplasms disrupt the normal function of healthy WBCs within the lymphatic system, decreasing effectiveness of the immune & lymphatic systems in fighting infections
- Signs/symptoms: fatigue, lymph node enlargement (painless), B symptoms (unexplained fever, drenching in night sweat, weight loss), severe itchiness, abdominal symptoms, cough/chest pain/mediastinal mass
24
Q
Briefly describe the pathophysiology, including signs & sypmtoms, of myeloma
A
- Pathophysiology: cancer of plasma B-cells. The malignant plasma cells grow into tumours within bone marrow- most commonly at multiple sites (multiple myeloma). It is more common after the age of 40. These myeloma cells also produce abnormal antibodies (paraproteins). Causes production of the faulty antibodies (paraproteins), various signals secreted by the myeloma cells and the crowding of the bone marrow with the myeloma cells, leading to various effects on the body.
- Signs/symptoms: Back pain, resp. tract infections, anaemia, renal failure, proteinuria, fractures, bone lesions, dehydration
25
Describe the phases of an acute infection and outline common signs & symptoms
1. Incubation: pathogen is replicating, but no signs/symptoms have developed.
2. Prodrome: initiation of signs/symptoms (typically mild & vague) while pathogen continues to replicate.
3. Illness: period of significant signs/symptoms (typically more severe) specific to the infection.
4. Decline: decline in signs/symptoms as elimination of pathogen enhances.
5. Convalescence: signs/symptoms disappear, infection has been contained/eliminated.
Signs & symptoms:
Fatigue, fever, weakness, reduced appetite, aches, loss of conc., localised signs of inflammation (redness, swelling, heat, plain, etc.), generally feeling unwell
26
Outline the benefits of fever during infection
1. kills or inhibits the growth of pathogens
2. decreases iron and zinc availability for pathogen growth
3. enhances chemical reactions and immune activity
27
For chlamydia & gonorrhea:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. Bacterial infections. Chlamydia can only replicate w/in host cells.
2. Transmitted via sexual contact (infects reproductive tract) or vertical transmission (infects eye, can lead to pneumonia w chlamydia).
3. Can be asymptomatic, but symptoms incl.: urethral/vaginal discharge, dysuria, painful intercourse (female), pelvic/abdominal pain.
4. Treatment: antibiotics
28
For tuberculosis
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. Bacterial infection; bacteria produces a waxy coat which protects it from the immune system; most commonly affects the lungs; macrophages engulf the bacteria but do not destroy them; leads to immunity.
2. Droplet transmission
3. Symptoms: fever, night sweats, poor appetite, weight loss, tiredness, persistent and productive cough
4. Treatment: multiple antibiotic drug therapy. Vaccination also available
29
For urinary tract infections:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. bacterial infections; multiple types of bacteria (most common is E. coli). Cystitis = inflammation of bladder, pyelonephritis = inflammation of renal pelvis and interstitium.
2. Transmission associated w bacteria already in/on the body whose growth becomes uncontrolled or which moves to another region (e.g. GI tract to urinary)
3. Cystitis: urinary freq. and urgency, dysuria, lower abdominal/back pain
Pyelonephritis: fever/chills, groin/back pain, general malaise, polyuria
4. Treatment: antibiotics
30
For helicobacter pylori infection:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. bacterial infection
2. transmitted via direct contact and waterborne
3. Appears that bacteria can stimulate gastric cell apoptosis and neutralise stomach acid causing inflammatory response.
4. Treatment: proton pump inhibitors and antibiotics
31
For HPV:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. 200+ varieties, specifically infect human epithelial cells (categorised by which cells they prefer to infect, e.g. cutaneous, mucous).
2. Transmitted via skin-skin contact (with infected epithelial cells) and some varieties sexual contact
3. Breaks in the epithelium allow HPV to attack the basal stem cells of the epithelial layers, causing uncontrolled cell growth of the epithelial cells.
Symptoms: warts and lesions, precancerous lesions, respiratory papillomatosis, carcinomas.
4. Treatment: removal of warts and precancerous lesions (physically or chemically), immune modifiers to boost immune system (remove infection on its own), most HPV infections go away on their own over time.
32
For herpes simplex virus:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. A variation of herpes virus. 2 types: HSV-1 (mainly oral) and HSV-2 (mainly genital)
2. Transmitted via direct contact with lesions or their secretions, and vertical transmission (HSV-2)
3. Primary infection occurs initially, then it becomes dormant in nerve ganglia w subsequent reactivation/recurrent infection.
Manifestations of active infection incl.: appearance of lesions (oral or genital), systemic symptoms (fever, headache, malaise), localised symptoms (pain, dysuria, itching, discharge)
4. Treatment: anti-virals. Prevention is avoidance of lesions and protected sex.
33
For varicella zoster virus (herpes virus):
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. Type of herpes virus. Causes chickenpox (varicella) in primary infection and shingles (herpes zoster) in a secondary.
2. Transmission is droplet and direct contact with vesicles.
3. Chickenpox symptoms: fever and malaise w disseminated itchy, vesicular rash. May lead to pneumonia, encephalitis and hepatitis.
Shingles: pain and eruption of vesicles in an area of skin supplied by one or 2 spinal nerves.
4. Treatment: chickenpox rarely treated unless severe or complications, but topical ointments alleviate the itch. Shingles can be treated w anti-viral medications, topical creams/lotions and/or analgesics.
Vaccines also available.
34
* *For viral hepatitis:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. Caused by a group of viruses (A, B, C, D or E) which cause inflammation of the liver and may lead to hepatocyte damage. A, B & C are most common forms.
2. Hep A: foodborne or waterborne transmission (via faecal contamination)
Hep B & C: contact w bodily fluids, sexual contact, vertical transmission
3. May be asymptomatic, all can cause acute infection. Hep B & C can lead to chronic infection and incr. risk of chronic liver disease, hepatic cancer and liver failure. Hep A is usually more mild infection, whereas Hep B and C can cause more severe infection.
Acute symptoms:
pre-icteric phase incl. fatigue/malaise, fever, headache, abdominal ache/pain, anorexia/nausea/vomiting
Icteric phase inc;. jaundice, fatigue, dark urine/light stools, liver tenderness and enlargement
Recovery phase: jaundice disappears, liver may remain large and tender, other symptoms diminish
Chronic infection usually doesn't involve the recovery phase, and liver function tests remain elevated after 6 months
4. Acute infection generally self-limiting and treatment typically supportive. Chronic is treated w antiviral drugs (suppress replication to prevent irreversible lever damage).
35
Outline the more common types of healthcare acquired infections (HAI)
- urinary tract infections
- surgical site infections
- central line acquired blood stream infection
- Methicillin-resistant Staphylococcus aureus (MRSA) infection
- Clostridium difficile infection
- pneumonia
36
* *For HIV:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. Retrovirus (2 types: HIV-1 and HIV-2) that infects immune system cells, leading to a decr. in immune function and incr. susceptibility to other infections/disease.
2. Transmission: contact with blood and reproductive secretions, vertical transmission (incl. breastmilk)
3. Initial infection (phase 1): acute symptoms incl. flu-like symptoms (headache, fever, sore throat, muscle/joint pain, fatigue, sores, etc.)
Latent period (phase 2) (approx. 10 years): asymptomatic
in this phase, virus proliferating w/in immune cells in lymph nodes, mostly T-cells. Inserts its own DNA into the cells DNA; triggers apoptosis of these cells and surrounding immune cells.
Over time this results in reduced immune system functioning, but also production of antibodies.
Once the level of CD4 cells is inadequate for sustained periods, AIDS develops bc no functional immune system (phase 4). AIDS incl. presence of opportunistic infections or cancer, which ultimately leads to death. Also accompanied by chronic disease symptoms e.g. wasting syndrome or recurrent fevers.
4. Treatment: combination or antiviral drugs (HAART), which slows progression of HIV and delay onset of AIDS.
37
For influenza:
- describe the infection
- outline the methods of transmission
- describe the pathophysiology of the infection, including signs & symptoms
- outline treatment & prevention options
1. 3 types of influenza virus: A, B and C, which cause resp. infection.
2. Transmission is droplet, direct contact and indirect contact.
3. Virus infects the upper resp. tract lining, initiating an inflammatory response causing systemic and localised symptoms. Particularly type A strains, replication of influenza virus often includes mutations that lead to different strains that the immune system doesn't recognise (hence repeated infections)
4. Treatment: prevention, incl. vaccination, hand washing and pulmonary hygiene.
38
Describe the different mechanisms of burn injury
1. Scalds: caused by hot liquids or steam
2. Flash and Flame: often deep burns, cause denaturation of proteins in the skin
3. Contact: caused by touching a hot object
4. Electrical: current is converted to heat as it passes through the body, damaging the tissue along its path.
5. Chemical: occur when skin is exposed to alkalis, acids or other corrosive chemicals. Chemical energy converted to thermal energy causing tissue damage.
6. Radiation: occur due to exposure to UV radiation from sunlight. Also radiotherapy treatments for cancer may cause burns.
39
Compare the tissue involvement in superficial, partial thickness and full thickness burns
1. Superficial (1st degree): epidermis layer.
- Pink colour, blisters and moist, capillary refill, sensation and hairs all present. Healing time <14 days, very painful.
2. Partial thickness (2nd degree): dermis layer.
- Mottled red or white colour, blisters mostly soft, sluggish/absent capillary refill, absent/distant sensation, few hairs present. Healing time >21 days.
3. Full thickness (3rd degree): hypodermis layer (fat, muscle and bone)
- White/tan/fawn/black colour, dry and leathery, no capillary refill, sensation or hairs. Healing requires second intention
40
Cite the determinants for grading burn severity
1. Extent of burn
2. Patient age
3. Burn wound depth
41
Describe the major considerations in burn therapy
- airway maintenance
- fluid resuscitation: Calculation of fluid replacement is commonly based on the Parkland formula (4 mL of intravenous solution (Ringer's lactate solution) × percentage of total body surface area burned)
- Large quantities of protein are lost as a result of a burn injury, increasing nutritional requirements.
- ain management is also an important aspect of treatment,
42
Local effects of burns
- Pain
- Vasodilation
- Increased capillary permeability (loss of albumin into interstitial space)
- Loss of fluids and electrolytes into interstitial space and environment
- Loss of heat due to conduction and evaporation
- Loss of protective skin barrier
43
Systemic effects of burns
- Hypovolaemia and burn shock (loss of circulating fluid vol.)
- Hyperpermeability of capillaries (vasodilation, release of inflammatory mediators, plasma leaks out of capillaries)
- Heat induced denaturing of collagen fibres (in interstitium, causing extravasation of fluid)
- Hypermetabolic state bc loss of skin integrity leads to loss of body temp (release of stress hormones: glucagon, cortisol, catecholamines)
- Suppression of insulin, GH and anabolic steroids
- Immune response to burn: infiltration of tissue w WBC, deficiency of neutrophils may cause fatal infections
- Loss of GIT barrier function
- Stress ulceration
- Bone marrow suppression
- Widespread whole body changes
- hyperkalaemia (Na moves into injured cells and potassium moves out)
44
First aid measures for burns
1. Remove patient from cause
2. Put out flames "stop, drop and roll"
3. Remove clothing in scalds
4. Airway maintenance and fluid resuscitation, give oxygen
5. Calm and reassure patient
6. Pain management is also v important
45
Pathophysiology of a burn wound
Jackson's burn wound model:
Burn wound has 3 zones of injury:
1. Zone of coagulation.
- Central area, closest to source of burn; nonviable tissue
- Coagulation of cellular proteins and destruction of microcirculation --> rapid cell death and necrosis
2. Zone of stasis (middle zone).
- surrounding the central area
- Slowed blood flow, decreased tissue perfusion (hypoperfusion and ischemia)
- Increased capillary permeability --> leakage of fluid into extravascular space.
3. Zone of hyperaemia (outermost area).
- surrounding the zone of stasis, contains viable tissue
- increased tissue perfusion
46
Define hypertonic
fluids where the solute concentration is higher than in the blood (and thus the solution also has less water than the blood)
47
Define hypotonic
fluids that have a lower solute concentration (are more dilute) than the blood
48
Define isotonic
solutions that have the same concentration of solutes as the normal plasma concentration.
49
Describe colloids
- Gelatinous solutions containing particles which can't cross the semi-permeable membrane
- Fluid remains in intravascular space
- E.g. albumin, dextran
50
Describe crystalloids
Clear fluids made up of water and electrolytes
51
Describe how the type of IV fluid given can alter the movement of fluid in body compartments
1. Saline (crystalloid) will cause immediate expansion of intravascular volume, but sodium will diffuse into interstitial space causing equilibrium (cannot move into ICF). Then, water will move from intracellular space to equalise osmolality in all 3 compartments.
2. Colloid stays in vascular space, increasing oncotic pressure (bc proteins). Water is then pulled into the circulatory system
3. Blood will remain in intravascular compartment, the other compartments are unaffected.
52
Describe the signs of dehydration and fluid overload
1. Dehydration (hypovolaemia):
- postural hypotension
- Tachycardia
- Absence of jugular pulse
- Decreased skin turgor
- Dry mucosae
- Supine hypotension
- Oliguria
- Organ failure
2. Fluid overload (hypervolaemia)
- Hypertension
- Tachycardia
- Raised JVP
- Oedema
- Pleural effusions
- Pulmonary oedema
- Organ failure
53
Name what you would use to replace the following fluid imbalances:
1. Loss of blood
2. Loss of plasma
3. Fluid resuscitation
4. Fluid loss
1. Blood
2. Colloid
3. Colloid and crystalloid
4. Crystalloid
54
Outline the effect that antibiotics have on the cell wall of bacteria
Bind to enzymes involved in the formation of cross-links in bacteria cell walls (transpeptidases).
By inhibiting the formation of cross-links, penicillins weaken the peptidoglycan structure causing the bacteria to lyse.
55
State the difference bw Gram +ve and Gram -ve organisms
- Gram negative bacteria don't pick up stains bc they have an additional outer membrane outside the cell wall.
- Gram positive bacteria do pick up certain stains bc they have a very thick peptidoglycan layer
56
Describe the different types of antibiotic drugs available for use
1. Sulphonamides: modification of energy metabolism
2. Penicillins: Inhibition of synthesis or damage to cell wall.
3. Cephalosporins: Inhibition of synthesis or damage to cell wall
3. Carbapenems: Inhibition of synthesis or damage to cell wall
4. Monobactams: Inhibition of synthesis or damage to cell wall
5. Tetracyclines: Inhibition of protein synthesis
6. Aminoglycosides: Inhibition of protein synthesis
7. Macrolides: Inhibition of protein synthesis.
8. Fluroquinolones: Interferes w DNA replication
607 Pathophysiology
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