Test 2 content Flashcards
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.
