WK 7- Renal and Haematological Emergencies Flashcards
What are the functions of the kidneys
- Excretion of waste products
- Acid base homeostasis
- Osomolality homeostasis
- BP regulation→ ie. Renin angiotensin system
- Hormone synthesis/metabolism
What are some causes of pre-renal failure
- Hypovolemia
- Hypotension→ Cardiogenic shock, sepsis, anaphylaxis
- Reduced effective circulating volume→ Generalised oedema secondary to cardiac failure, liver failure, nephrotic syndrome
- Renal hypoperfusion→ Renal artery stenosis, hepatorenal syndrome
What does pre-renal failure mean
failure resulting from anything that impairs blood flow to kidneys
What are some complications of renal failure
CNS→ Altered LOC, confusion, seizures
CVS→ Dysrhythmias, fluid overload
GIT→ Stress ulceration, ileus
Haematological→ Anaemia, platelet dysfunction
Metabolic→ Hyperkalemia, hypocalcemia, metabolic acidosis
Immunological→ Infection, poor wound healing
What are some renal causes of renal failure
Vessels
→Large: renal artery thrombosis/embolism/dissection, renal vein thrombosis
→Small: vasculitis, malignant hypertension, thrombotic microangiopathy (HUS/TTP)
-Glomeruli: Glomerulonephritis
-Renal tubules→ Acute tubular necrosis- can be ischemic or Cytotoxic – pigments, drugs
-Renal interstitial tissue→ Acute tubulointerstitial nephritis
What are some causes of post-renal failure
Internal obstruction→ Stone, clot, casts, crystals
External–> compression→Prostatomegaly, tumour, haematoma
→ can be relieved by indwelling urinary catheter
How is acute renal failure managed
Treat reversible causes
- Pre-renal→ correct hypovolemia, hypotension, anaemia (give blood transfusion)
- Post-renal→ IDC, SPC or nephrostomy tube for higher obstruction
- Avoid secondary insults→ avoid non-steroidals, amino glycosides→ these worsen renal failure
- Maintain urine output
- Treat complications→Hyperkalemia Tx, Renal Replacement Therapy (haemodialysis for chronic renal failure patients)→ complications mainly occur chronic renal failure
- Specific treatment for underlying cause
What does hyperkalemia cause? How can it be fatal?
-Causes hyperpolarisation/repolarisation of the cell membrane leading to difficulty in initiating an action potential-> causes dysrhythmias (potentially life threatening), muscle weakness
What ECG changes are seen in a person with hyperkalemia
Peaked T wave, broad QRS, shortened PR, flat/or no P wave
-over time will become sinusoidal
How is hyperkalemia treated
-Stabilise cardiac membranes→ calcium gluconate 10ml→ give calcium only to pt with abnormal ECG or K+ greater than 7.5
-Shift K into cells→
-Nebulised salbutamol 20mg→ shifts K intracellularly
-IV actrapid (insulin)
-IV NaHCO3 100mmol
-Enhance elimination of potassium–>
PO/PR resonium 50g→ binds K in gut and creates osmotic gradient that pulls K out of the gut and excretes
-IV frusemide diuresis→ useful in fluid overload in pt
-Renal replacement therapy- Dialysis
What conditions lead to chronic renal failure
Diabetes, reflux neuropathy, -Glomerulonephritis, Polycystic kidneys, Renovascular, Predominantly renal causes
How is chronic renal failure managed
- Dialysis→ Haemo vs Peritoneal (can do at home→ flood the peritoneal with diasolate-> body will slowly calibrate on its own)
- Protein + fluid restriction
- BP control→ tend to be hypertensive, so are on multiple anti-hypertensives
- Supplements
- Ca, vit D, Fe, PO4 binders, multivitamins
- Erythropoietin→ stimulates RBC formation
What is haemostasis
-a constant process of clot formation and clot lysis→ so there is no abnormal thrombosis
What are the 3 processes of haemostasis
-Vasoconstriction, platelet plug formation and coagulation
What 3 factors contribute to abnormal bleeding
→vessel injury–> severing the vessel can cause haemorrhage (cannot be repaired via platelet plug)
→ platelets; thrombocytopenia, platelet dysfunction (ie. Aspirin/clopidogrel)
→ coagulation cascade; coagulopathy
What are the two ways in which a person can get coagulopathy
Congenital or acquired
How can coagulopathy be congenital
ie. inherited syndromes like haemophillia
How can coagulopathy be acquired
→Inadequate synthesis; Liver disease, vit K deficiency
→Coagulation inhibition; Antibodies, drugs (ie. Warfarin, novel oral anticoagulants)
→Coagulation factor consumption;
Disseminated intravascular coagulation, snakebite
How is major bleeding managed
Resuscitation→ DRABCD
-Early source control→ stopping the bleeding
→ Physcial measures: pressure (ie. Lower limb bleed-pressure on femoral artery), elevation, splinting- helps tamponade the bleeding and alleviates pain
→ Surgical haemostasis: damage control surgery → controlling bleeding and correcting haemodynamics initially
→ Specific medical treatment: eg- upper GI bleed= PPI+ octreotide, antivenom for snakebite (Binds to venom and stops progression of coagulopathy)
What is tranexamic acid
anti-fibrinolytic derivate of lysine that interferes with the normal fibrinolysis process and competitively inhibits activation of plasminogen through reversible interactions with lysine-binding sites on the enzyme
How does saline make coagulopathy worse in a major trauma
- dilutes clotting factors- prolonging haemorrhage
- has no oxygen carrying capacity-> further decreases perfusion to tissues
What is the ratio of RBC:FFP:Plts used in major trauma
1:1:1
How much blood is in an;
- adult
- child
- infant
Adult 70ml/kg = approx 5L
Child 80ml/kg
Infant 90ml/kg
If the pH is below 7, what will not clot effectively
-what does this mean for management
- Platelets do not clot below a pH of 7
- have to control acidosis before giving transfusion
What factors do not work in low temperatures
- Clotting factors
- need to correct hypothermia before transfusion
What are the 2 definitions used for a massive transfusion
→ Replacement of > ½ blood volume (5units RBC) within 4 hrs
OR
→Replacement of full blood volume (10units RBC) within 24hrs
What is serum
-is essentially plasma (has proteins, water, hormones) just without clotting factors
What is plasma
contains proteins, water and other solutes (like clotting factors and hormones)
What complications can arise from a massive transfusion
- Hypothermia→ if you don’t warm products, can become hypo
- Acidosis
- Haemodilution→ if blood products have lower cellular content
- Consumption of clotting factors + platelets
- Use of fractionated blood products
- Disseminated intravascular coagulation
- Coagulopathy + microvascular bleeding
The ureters travel from the kidney toward the bladder in close association with what muscle?
Psoas major
How long are the ureters (approx)?
25-30 cm
What is the narrowest part of the urogenital tract? (i.e. where renal stones are most likely to get stuck)
- Ureteropelvic Junction (UPJ)→ anatomical location where the inside of the kidney connects to the ureter→ occlusion of stone causes colic pain
- as the ureter enters the pelvis and crosses over the common iliac artery bifurcation
- at the vesicoureteric junction (VUJ) as the ureter obliquely enters the bladder wall
The hilar of each kidney is near the transpyloric plane. At what level is the transpyloric plane?
-L1 vertebral body→ cuts halfway through the pylorus
Where would you expect to feel pain from the kidney
Loin to groin→ begins below ribs and radiates towards the groin
Where would you expect to feel pain from the ureter
flank pain on affected side/loin to groin
Where would you expect to feel pain from the urethra
suprapubic regon
Where would you expect to feel pain from the bladder
suprapubic region
Why can urogenic pain be either colicky or constant
- these structures are hollow viscous organs that have peristaltic waves passing through→ if a stone is moving, it will causes colicky pain due to the peristaltic waves
- constant pain is caused by inflammation→ pyelonephritis
What are some complications of catheterisation
-urinary tract infection, bladder spasms, blood/debris in the catheter, damage to the urethra, formation of scar tissue, bladder stones, injury to bladder or rectum
What is the role of the kidney in the renin-angiotensin system?
releases renin from juxtagolmerular cells→ renin converts angiotensinogen to angiotensin 1 so that it can eventually can be converted to angiotensin 2→ angiotensin 2 acts to increase BP through vasoconstriction, release of aldosterone, reabsorption of Na+, ADH release
What is the action of aldosterone
- Aldosterone is a type of steroid hormone that acts primarily in renal collecting ducts to stimulate reabsorption of Na+ as well as secretion of K+ and H+→ increases BP
What blood group is a universal donor
O- has no surface antigens
What blood group is a universal recipient
AB+ has no preformed antibodies
In trauma, what three factors contribute to coagulopathy?
- Hypothermia, coagulopathy/consumption, acidosis
- these factors contribute to acute coagulopathy of trauma/shock→ hypothermia causes decreased clotting factor activity, acidosis prevents platelet function, coagulopathy can cause further bleeding and acidosis
What is the MOA of frusemide
inhibit basolateral Na+/K+/2Cl-pumps in the ascending limb of the loop of Henle
- results in marked and rapid decrease in Na+ an Cl- reabsorption causing increased uresis and reduced BP
- avoid in those with low blood volume/dehydration
Which of the following is true regarding the hilum of the right kidney
- it is at the level of the lower border of L1
- it is deep to the transpyloric plane
- it is at a higher level than the hilum of the left kidney
- it moves with respiration
1, 2 and 4
Where would the pain from a renal calculus lodged at the ureto-vesical junction usually be felt
- Loin
- groin
- scrotum
- radiating from loin to groin
Groin
- stone higher up will have to move through the ureter-> causes visceral pain
- when stone becomes stuck it becomes painful around the groin
- those that are stuck in the bladder neck cause pain to radiate to the penis/scrotum
What kind of pain (visceral or somatic) does renal colic cause
visceral
Which of the following is typical of renal colic
- patient can’t get comfortable
- sharp pain, worse with movement
- peritonism
- fever
pt can’t get comfortable
-peritonism indicates fluid/blood in peritoneum which is made worse by pressure
Which of the following would cause pre-renal failure
- glomerulonephritis
- acute tubular necorsis
- renal artery stenosis
- prostatomegaly
renal artery stenosis
Which of the following would be most likely to cause post-renal failure
- glomerulonephritis
- renal calculi
- cervical cancer
- bladder calculus
cervical cancer–> invades bladder neck
Which of the following is a consequence of chronic renal failure
- tetany
- bleeding tendency
- clotting factor deficiency
- dehydration
tetany and bleeding tendency
- tetany due to electrolyte imbalances (hypocalemia)
- bleeding is due to; coag factors not working (acidotic),
Which of the following applies to group A pos blood
- group A antigen and group a antibody
- group A antigen and group B antibody
- group B antigen and group B antibody
A antigen and B antibody
Which of the following is universal donor
- O pos
- O neg
- AB pos
O neg
