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SA Emergency > Final Exam > Flashcards

Final Exam Flashcards

1
Q

More hydrogen means a - pH

A

Lower ph and vice versa

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2
Q

Acids - protons, bases - protons

A

Acids donate a proton (they have more to give ), bases accept a proton and combine with free hydrogen ions

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3
Q

Describe homeostasis in terms of acid base

A

Normal pt is 7.4, respiratory and metabolic systems maintain normal pH

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4
Q

Is HC03 an acid or base

A

A weak base ready to accept protons

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5
Q

Is PCO2 an acid or base

A

Acid ready to donate hydrogens

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6
Q

What does co2 combine with in the biologic buffer system

A

Combines with water (water in donate a hydrogen)

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7
Q

What should you ask yourself if there is an acidemia ( ph below 7.35) or alkalemia ( ph above 7.45)

A

Acidemia - is there too much acid or not enough base
Alkalemia - too much base or not enough acid

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8
Q

Acidemia with too much acid (a high CO2) indicates

A

Respiratory acidosis - respiratory system controls co2

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9
Q

Acidemia with not enough base (low HCO3-) indicates

A

Metabolic acidosis

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10
Q

Alkalemia with too much base (high hco3 -) indicates

A

Metabolic alkalosis

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11
Q

Alkalemia with not enough acid (low co2) indicates

A

Respiratory alkalosis

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12
Q

What are 5 differentials for a metabolic acidosis (not enough base)

A

DKA, lactic acidosis , uremic acidosis, ethylene glycol toxicity, aspirin toxicity (think klue)

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13
Q

What are differentials for a metabolic alkalosis (too much base - high hco3)

A

GI obstruction until proven otherwise

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14
Q

What are differentials for a respiratory acidosis ( too much cO2)

A

General Anesthetics , opioids, neuro conditions (cns, cervical spinal disease, LMN ), fatigue

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15
Q

What are differentials for a respiratory alkalosis (too little co2)

A

Severe hypoxemia , mild anxiety, CNS disease, severe hyperthermia, iatrogenic

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16
Q

What makes up the lower urinary tract

A

Bladder, urethra, caudal ureters, prostate in males

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17
Q

Will a UTI cause an obstruction

A

Never - but you could have a UTI secondary to an obstruction

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18
Q

What are common causes of lut signs in dogs

A

UTI, stones, mass/cancer

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19
Q

What are common causes of LUT signs in a cat

A

Idiopathic cystitis (mucous plug) , stones, mass/cancer - cats rarely get UTIs

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20
Q

What will you often see in a history of LUT signs

A

Irritation/inflammation - pollakiuria, stranguria, dysuria, accidents, hematuria - if obstructed will locally see systemic signs and the patient will feel sick

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21
Q

What is the major difference in LUT signs with obstructive versus not obstructive causes

A

Obstructive will feel systemically ill, non obstructive will not - also obstructive will cause a large firm bladder

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22
Q

What are differentials of a small firm bladder with LUT signs

A

UTI, stones, idiopathic cystitis, tumor

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23
Q

What are differentials for a large firm bladder and LUT signs

A

Obstruction or tumor

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24
Q

What is the best way to diagnose a UTI

A

Urine culture with sterile urine from a cystocentesis - urinalysis can be misleading

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25
Q

What are you looking for on rads for LUT signs

A

Radio opaque urolithiasis / stores

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26
Q

What are you looking for on ultrasound of LUT signs

A

Radiolucent uroliths, masses, clots , free fluid, dilated ureters or kidneys

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27
Q

What is almost always the case in cats with LUT signs, especially if they’re male

A

Idiopathic cystitis - if female more likely stones

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28
Q

A urine culture is never

A

Wrong

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29
Q

What are the steps in treating an obstruction causing LUT signs

A

Stabilize / diagnostics , then unblock ,more diagnostics if needed, definitive treatment

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30
Q

What are the steps to treating non obstructive lut signs

A

Stabilize (not usually needed), diagnostics, treatment

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31
Q

What can often mask the signs of shock in cats

A

Hyperkalemia - affects and distorts heart rate

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32
Q

Do you place a urinary catheter or an IV catheter list in a blocked cat

A

IV catheter - need blood to check electrolytes like potassium in case there is hyperkalemia (you can’t stabilize a patient without addressing the hyperkalemia)

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33
Q

Can u give fluid therapy to a blocked patient with LUT signs to stabilize them

A

Yes for a short time - 5 to 10 minutes ok, will not rupture the bladder and every animal with obstruction like this has some sort of kidney injury so need to keep this from getting worse

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34
Q

What can you use for hyperkalemia therapy

A

Calcium gluconate to stabilize the electrical activity in the heart, not to change the potassiumlevel

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35
Q

What can you give to drive potassium into the cells

A

Insulin, dextrose (to prevent hypoglycemia ), bicarbonate, injectable bronchodilators

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36
Q

How does hyperkalemia affect cardiac function

A

Increases the resting membrane potential making it harder to reach, causing issues with contractility I irregular rhymes like still standstill, etc

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37
Q

What can you give to help restore the difference between resting and threshold potentials that was disrupted by hyperkalemia

A

Calcium - will buy you time but will not address the hyperkalemia

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38
Q

What are 2 general options to treat hyperkalenia in a blocked patient

A

Give drugs to drive potassium into the cells (bicarb, insulin, albuterol) or increase potassium excretion by unblocking and giving more fluids (dilute it out basically)

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39
Q

What’s important to remember when giving pain management/sedation to a patient with hyperkalenia

A

Want it to be CV sparing because the heart is already being negatively affected by potassium - options are ketamine, midazolam , alfaxalone, etc

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40
Q

What is common to see post obstructive divresis / post unblock in

A

Polyuria in excess, some degree of anotemia due to kidney damage - polyuria is a way for the kidneys to recover but you need to keep up with losses

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41
Q

What is the risk of antimicrobial post unblocking if there is an indwelling urinary catheter

A

Increased risk of resistance if indwelling urinary catheter

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42
Q

What empiric antibiotics are often used for UTIs

A

Amoxicillin - 3 to 5 days (case dependent)

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43
Q

Feline idiopathic cystitis if often treated with

A

Time and comfort - pain med, antianxiety, first time free but after then do rads to further diagnose

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44
Q

What stones are often seen in young toy breeds

A

Urate stones - shunt

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45
Q

Describe uroabdomen

A

Urine free within peritoneum causing pain peritonitis, life threatening often caused by trauma but could be a ruptured tumor , definitive treatment with surgery

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46
Q

How can you diagnose a uroabdomen

A

Compare peripheral creatinine and potassium to effusion - if abdominal potassium is 40% higher in the effision or if the abdominal creatinine in the efferent is twice the concentration as peripheral blood then uroabdomen woabdamen is indicated

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47
Q

What should not be used to diagnose uroabdomen

A

Bun - it diffuses rapidly

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48
Q

How do you treat uroabdomen

A

Drain wine with a peritoneal drainage catheter and keep bladder small with indwelling urinary catheter

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49
Q

Describe Kirbys rule of 20

A

Monitoring checklist for systemic assessment of the critically ill patient - combo of physical exam parameters and diagnostic tests

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50
Q

What is the benefit of Kirbys rule of 20

A

Minimizes the chance of missing significant abnormalities

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51
Q

What is meant by a point of care test

A

Cage side to get essential results quickly

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52
Q

What are 4 walls to formulate an effective monitoring plan

A

Anticipate potential complications, interpret physical exam and diagnostic findings, establish target endpoints (treat p not number) I implement timely changes in treatments ( life threatening first)

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53
Q

What is the gold standard poc test for hypoxemia (pao2 less man 80)

A

Arterial blood gas - pulse ox second best

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54
Q

Where do you take a pulse ox (saturated oz)

A

Non pigmented skin

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55
Q

Relate cyanosis and hypoxemia

A

Cyanosis is a late sign of hypoxemia and death may precede cyanosis it patient is anemic

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56
Q

What values indicate hypoventilation and how is it determined

A

PaCo2 over 45 (severe if over 60) - determined with co2 production divided by alveolar ventilation

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57
Q

How do yo measure ventilation

A

Arterial blood gas, venous blood gas, end tidal co2

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58
Q

Vomiting comes from the - regurg comes from -

A

Vomiting from brain, regurg from esophagus

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59
Q

What are signs of vomiting

A

Nausea, agitation, drooling, lip smacking, retching (abdomen use, hacking)

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60
Q

What are signs of regurgitation

A

Passive, often when changing positions or walking, hard swallowing , no warning and no nausea

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61
Q

Describe signs of large bowel diarrhea

A

Urgency, straining / tenesmus, mucus / frank blood

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62
Q

Describe small bowel diarrhea

A

No urgency , possible increased frequency, no straining, melena

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63
Q

Can ew differentiate type of diarrhea through volume or consistency

A

No

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64
Q

Can ya differentiate vomiting versus regurg based on contents

A

No

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65
Q

What on blood gas would indicate an obstruction causing diarinea or vomiting

A

Metabolic alkalosis

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66
Q

Describe hemorrhagic gastroenteritis and now do you diagnose

A

Collection of signs , idiopathic, elevated PCV with low or normal TS suggestive, diagnosis of exclusion ) no specific test to anti

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67
Q

Kidneys are - but are not -

A

Kidneys - filter bad stuff and hold onto water to prevent dehydration (or get rid of later to prevent fluid overload)

68
Q

Describe prerenal azotemia

A

Problem before the kidneys - usually dehydration or hypovolemia, urine should be concentrated because kidneys are holding the water they do have

69
Q

Describe post renal azotemia

A

Problem cores after the kidneys - lower urinary tract obstruction or rupture, base on physical exam and imaging

70
Q

With how much nephron loss will you see an azotemia

A

75% nephron loss - will have isothenuria with 67% loss

71
Q

What’s the difference between SDMA and CK as markers of renal function

A

CK affected by muscle loss , SDMA has a wider range

72
Q

Describe signs of acute kidney injury

A

Acute onset, quite sick despite moderate azotemia, good bcs, no anemia, kidney pain and enlarged kidneys

73
Q

Describe chronic kidney disease

A

Insidious unset, stable despite severe azotemia, anemia, muscle wasting, small and irregular kidneys

74
Q

If you suspect azotemia, what tests should you do

A

USG and culture are top priority - urinalysis not worth it, assume some degree of pre venal azotemia

75
Q

Do fluids treat kidney injury

A

No - with AKI you need to treat the underlying causes

76
Q

Why are fluids a go to when treating AKI

A

Could help treat the prerenal compartment of AKI and help patient feel better / prevent further complications

77
Q

Does dialysis treat kidney disease

A

No - fills in to the kidneys while they are sick

78
Q

What happens when you refrigerate fresh whole blood

A

Platelets give up basically - unredigerated fresh whole blood is good for 24-48 hours (keeping platelets stable)

79
Q

What happens when you centrifuge fresh whole blood

A

You get plasma which can be frozen for a year or packed red cells which can be frozen for 2 weeks

80
Q

At what PCV do you need to transfuse

A

None - depends on clinical signs and suspicions of blood loss states a while for PCV to change with blood loss (quicker if uw give fluids)

81
Q

Blood typing should always be done

A

In cats - they develop all antibodies to blood types that aren’t theirs, dogs get one transfusion before you need to crossmatch

82
Q

When would you transfuse whole blood

A

When you reed red blood cells and plasma - coagulopathy due to rodenticide, blood loss anemia

83
Q

Why are packed ABCs used more commonly

A

Lower risk of transfusion associated circulatory overload (taco)

84
Q

What can you give if you need fresh whole blood but don’t have it

A

Packed RBCs and fresh frozen plasma - both of these are easier to store

85
Q

How much of a blood product should you give when transfusing

A

Start with 10 ml/ kg then reassess

86
Q

When should you not transfuse an anemic patient

A

If they aren’t showing signs of anemia / monitor heart rate instead (better than PCV)

87
Q

What are indications for using plasma

A

To replace missing clotting factors (contains the most proteins), part of a massive transfusion with packed red blood cells , maybe when reduced effective circulation but no evidence

88
Q

When should you almost definitely cross match before transfusing

A

If time and if they’ve had previous transfusions

89
Q

When do you stop transfusing

A

When clinically the patient is better or stable, check clotting times, based on the patient not the numbers

90
Q

How do you determine replacement fluids

A

Body weight in kg times percent dehydrated - if not eating and vomiting, safe to assume 5% dehydrated

91
Q

If you have an azotemic patient and you suspect CKD what do you do

A

Need to know if it is an acute exacerbation or progression of CKD - collect a urine sample for culture because CKD patients more at risk for pylorephritis, consider metal obstruction or nephrotoxins, assume some degree of presenal azotemia and dehudation because the kidneys cant concentrate

92
Q

How do you treat CKD

A

Manage clinical signs, treat secondary AKI if present, antinausea, phosphorous binders, dietary managent1 blood pressure management

93
Q

Will dehydration help treat CKD

A

No just like AKI - will help treat or prevent dehydration and help patient feel a little better ‘

94
Q

Why do CKD patients become dehydrated

A

They can’t concentrate wire and develop an obligatory polyuria and then polydipsia to keep up with losses I but sometimes they just can’t drink enough - so need either at home sub Q fluids or esophagostomy tube

95
Q

What are pros and cons of at home subcutaneous fluids

A

Inexpensive and easy but does have excess salt and risk of patient intolerance and lack of client ability

96
Q

What are pros and cons of an esophagostomy tube

A

More physiologic and no extra salt , improved patient tolerance, easy to give, can give mediations this way too, - but does cost more upfront and require a procedure to place the tube , risk of complications like a stoma infection, dislodgement of tube or esophageal strictures

97
Q

What is a stoma infection

A

Information and swelling around an opening (like with an esophagostome tube)

98
Q

What do you need to consider wha giving a CKD patient antinasusea meds to eat

A

Need to insider QOL - once they don’t want to eat they are close to the end - should you use an E tube to keep the patent alive if they don’t want to eat?

99
Q

Why are phosphorus binders often used to treat symptoms of CKD

A

Phosphorous depends on GFR and tends to follow bun and CK (so phosphorous is high in azotemic patients) - high phosphorous an mike the patient nauseous and uncomfy and on worsen calcium and then kidney function - 50 give phosphoras binders to prevent these side effects

100
Q

Are prescription diets recommended to treat kidney disease

A

CKD yes - can slow progression and extend life expectancy, not really with AKI

101
Q

Why should you monitor blood pressure in CKD patients

A

Hypertension common in CKD patients and hypertension worsens kidney function - treat if persistent and severe hypertension

102
Q

How do you often treat hyper tension in CKD patients

A

Enalapril and amlodipine

103
Q

A cat ingested large amounts of Lillies - do you give then hydrogen peroxide to induce vomiting

A

No never - hydrogen peroxide in cats can cause gastritis with terrible uceration or fatal henormagic gastritis

104
Q

Is hydrogen peroxide still the recommendation to induce vomiting in dogs

A

No causes significant irritation of the esophagus and stomach causing partial ulceration

105
Q

What is recommended in dogs now to induce vomiting - which works better

A

Apomorphine (compounded to be an IV injection) or clevor eye drops, hydromorphone - apomorphine less likely to need a second dose

106
Q

What is recommended to induce vomiting in cats

A

Alpha 2s like dexmedetomidine and xylazine, hydromorphone extra label

107
Q

What is the number I thing you need to do when a patient ingests toxins

A

Get it out of the body quickly - need to made sure p can protect their airways and has an appropriate mention before inducing vomiting

108
Q

Most toxins warrent - unless otherwise noted

A

Warrent emesis - especially if concern for foreign body obstruction, note mention and make sure p is stable first

109
Q

When do you not induce erresis

A

Corrosive or caustic agents , over 6 hours post ingestion, predisposed to aspiration , poor mention or neuralgic status

110
Q

Which adsorbent works well for decatomination

A

Activated charcoal /toxiban - single dose used for most intoxicants , risk of hypernatremia after multiple doses

111
Q

Why is sorbitol often given with activated charcoal

A

Rapid transit through the gut

112
Q

What can ya do to decontaminate comatose patients or patient where emesis did not work

A

Gastric lavage

113
Q

What do you give in an enema for decontamination

A

Warm tap water, lactulose , dawn or ivory dish soap

114
Q

How do you treat toxic ingestions

A

Decontaminate S treat clinical signs, decontaminate if possible, intra lipid therapy, minimize absorption with enemas

115
Q

Most toxins cause - unless otherwise noted

A

Git signs even if git is not the target damage organ

116
Q

What organs are targeted by chocolate toxicity (methylxanthines - caffeine, theobromine/theophylline)

A

Git specifically , vomiting is often seen - heart and brain affected too

117
Q

What are clinical signs of chocolate toxicity and when do they occur

A

Vomiting, tachycardia, tesessness, hyper excitation, agitation - signs occur 1-4 hours post ingestion

118
Q

What is the treatment for methlyxanthine toxicity (chocolate)

A

Activated charcoal with sorbitol, ECG , fluids - often just reed one dose and then they’re fine / really good prognosis if decontamination happened quick enough

119
Q

Describe clinical signs of NSAID toxicity

A

GI - abdominal pain, hematamesis, melena
renal - pu/pd, decreased urine;
hepatic damage- is idiosyncratic and not dose dependent!
Nerve - seizures, obtunded
Heart - hypovolenick shock

120
Q

What signs can result with COX 1 inhibition from NSAID toxicity

A

Gastric ulcers, GI bleeding

121
Q

What signs can occur with cox 2 inhibition from NSAID toxicity

A

Hypertension, water and sodium retention, AKI

122
Q

Are you likely to see gastric ulcers from NSAID toxicity

A

Maybe but more likely to see with chronic NSAID use

123
Q

How do you treat NSAID toxicity

A

Ulcer prevention, renal support (fluids and monitor urine + weight), treat hypovolemic shock- intravenous lipids, dialysis if needed

124
Q

Does sucralfate treat gastric ulcers

A

Binds defects but does not protect the mucosal lining - so keeps present defects from worsening but doesn’t paint formation of new ones

125
Q

What is the prognosis for nsaid toxicity

A

Worse if decreased to no urine output, renal failure ór ulceration requiring surgery - neurodeficits will usually get better

126
Q

What are clinical signs of xylitol toxicity

A

Weakness, depression, ataxia, tremors, seizures hepatic /hematologic like icterus, melena, petechia ,remarriage, hypoglycemia due to increased insulin release from pancreas, hepatic failure if ingested large amants

127
Q

How do you treat xylitol toxicity

A

Dextrose for emergent seizure patients and for hypoglycemia, nacelyleistine for hepatic necrosis, monitor pt and att

128
Q

What are clinical signs of wild mushroom toxicity

A

Unexplained acute signs - hypersalivation, ataxia, v/d. Dull mention, tremors, agitation, vocalization

129
Q

Most wild mushroom toxicity can be treated by decontamination except

A

Amanita and galerinia - both are hepatotoxic and need hepatic support

130
Q

Sago palm toxicity is similar to _ and cause -

A

Xylitol toxicity - causes hypersalivation, pu/ pp, melena, jaundice, seizures, ataxia, dull mentation

131
Q

Who an d what is most affected by sago palm toxicity

A

Dogs most affected - all parts of plant toxic and target git, liver and CNS

132
Q

What is the primary target organ of marijauna /THC / CBD? What clinical signs are seen?

A

Nervous system /brain - causes lethargy, hyperesthesia, ataxia, agitation, seizures, comatose - can also cause bradycardia and hypothermia

133
Q

When do signs of marijauna toxicity occur

A

20-30 minutes after exposure and can last 2-3 days

134
Q

Do animals have to ingest the marijauna for it to be toxic

A

No - Can just be from inhalation

135
Q

How do you treat marijauna toxicity

A

Benign neglect usually, emesis with AC + sorbitol for large ingestion amounts

136
Q

What shard you rapidly use for marijauna toxicity

A

Rapid use of intralipids when clinical - improves in 30 mins to 1 hour

137
Q

What are signs of seroton uptake inhibitors toxicity and when do they occur

A

Tachycardia, neuro signs ( ataxia, disorientation, absent menace, tremors) 1 occurs 1-2 hours after ingestion

138
Q

How do you treat ssri toxicity

A

Acepromazine, methocarbomal for tremors; cryptoheptdine as serotonin antagonist - supportive therapy leads to a good prognosis

139
Q

What clinical signs do you see from rodenticide toxicity and when do you see them

A

Green discolored feces, neuro signs , nystagmus - an see signs as early as 24 hard but can progress to 2 weeks

140
Q

What is the most common rodenticide toxicity

A

Bromethalin

141
Q

How to you treat rodenticides

A

No antidote - AC, intralipids, seizure control, mannitol - severe neurologic signs bad prognostic indicator but if my only develop mild signs they have a better prognosis

142
Q

What clinical signs do you usually see with pyrethoids

A

Most commonly see in cats (flea and tick ) - neurotoxic, clinical signs in 1-2 hours

143
Q

How do you diagnose pyrethroid toxicity

A

Lbs consistent with muscle trauma - kidney injury, dehydration, hyperthermia

144
Q

How do you treat pyrethroid toxicity - common in cats

A

Bath if applied topically, seizure management, intralipids therapy to protect nervous system

145
Q

What are signs of vitamin. D toxicosis

A

Nephrotoxic - pu/pd, uremic ulcers, GI signs, near signs, hyperkalenia leading to kidney failure

146
Q

How is vitamin D toxic

A

Cholecalciferol converted to calcitriol in is dreys which decreases calcium and p excretion and increases gut aborpken

147
Q

How do you treat vitamin D toxicosis

A

Promote decreased renal absorption and increased excretion to remove excess calcium- phosphate binders to decrease git absorption of calcium and phosphorous

148
Q

What are clinical signs of grape/raisin toxicity and what is their MOA

A

Renal / nephrotoxic - pu/pd / standard git effects - idiosyncratic toxicity

149
Q

How do you treat grape toxicity

A

Control symptoms of AKI and azotemia (like with vitamin D toxicosis) - monitor for hypertension which makes kidney injury worse

150
Q

Describe signs of ethylene glycol toxicity and when they occur

A

Nephrotoxic - urine dribbling, near (1-6 hours), drunk phase that resembles marijauna1 ataxia, blindness - occur within 12-24 hard

151
Q

How do you treat ethylene glycol / antifreeze toxicity

A

Dialysis, ethanol - treatment has to be sought in 6 hard or prognosis is poor

152
Q

What is the MOA of Lilly toxicity

A

All parts of the Lilly is toxic - affects the glomensus and fuses obstruction of the tubules

153
Q

What are clinical signs of Lilly toxicity - when do you see signs

A

Nephrotoxic - pu/pd, drooling, seizures, see signs in 24 hours

154
Q

With what nephotoxic substance do you often see hypercalcemia

A

Vitamin D toxicosis

155
Q

Describe signs anticoagulant rodenticide toxicity

A

Multi compartment bleeding, green feces, dyspnea - signs of bleeding may not be seen for up to a week after exposure

156
Q

When should you recheck coagulopathy times after treating an anticoagulant rodenticide poisoning with vitamin K

A

48 - 72 hours after stopping the vitamin K

157
Q

What is important to remember about acetaminophen toxicity

A

Some contain codeine so might need to treat for 2 toxicities

158
Q

What are clinical signs of acetominpher toxicity

A

Cyanosis due to methb 1 dull mention, signs of liver failure in 2 days

159
Q

What is the prognosis for acetaminophen toxicity

A

Poor due to toxic metabolites - often in liver failure before you see cyanosis

160
Q

What are toxin differentials for a coagulopathy

A

Vitamin K rodenticide , hepatotoxic substances, NSAIDs

161
Q

What are toxin differentials for azotemia

A

Lillies in cats, ethylene glycol, raisins I grapes, NSAIDs

162
Q

What are toxin differentials for increased liver enzymes

A

Sago palm , xylitol, acetaminophen , amatoxic mushrooms, NSAIDs

163
Q

List primary hematologic toxins

A

Anticoagulant rodenticides , acetaminophen

164
Q

List primary nephrotoxic substances

A

Vitamin D toxicosis, grapes I raisins, ethylene glycol/antifreeze , Lillies in cats

165
Q

List primary neurotoxic substances

A

Marijauna ,ssris , neurotic rodenticides (bromethalin), pytethroids

166
Q

List multi organ target toxins

A

Methylxanthines (chocolate) / NSAIDs / xylitol, wild mushrooms, sago palm

SA Emergency (3 decks)

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