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Clinical Sciences 1 > Clinical Reasoning + Endocrine Hormones Review > Flashcards

Clinical Reasoning + Endocrine Hormones Review Flashcards

1
Q

premature closure

A

concluding evidence gathering and making a diagnosis prior to thorough reflection on all data. commonly associated with pattern recognition

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2
Q

false consensus

A

form of premature closure. offer limited analysis/information because you believe that others have reached an identical conclusion

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3
Q

confirmatory bias

A

tendency to seek or favor data that confirms one’s preferred diagnosis while ignoring or disregarding data that would disfavor the diagnosis

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4
Q

unintentional sequestration of data

A

pertinent information is unintentionally omitted by someone on the team; eg clinical sign, previous medical history, etc

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4
Q

illusory transactive memory system

A

related to unintentional sequestration of data- provides medical team with a deceptive sense of security that because you’re working with a team, someone before you got all the data that you need. “someone must’ve read the chart”

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4
Q

contagious illusion

A

respect for authority or desire for consensus allows data to be interpreted as valid by others; eg a supervising clinician states that a collection of clinical signs means the patient has _____ disease

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4
Q

what medical error can be summarized to “someone must have read the chart”?

A

illusive transactive memory system

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5
Q

selective perception

A

expectations influence your senses such that you can feel, hear or see something that you expect to hear

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6
Q

recency effect

A

the most recent events in the patient’s medical history or disease are more heavily weighted than the events that occurred earlier

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6
Q

what medical error can be summarized in “well the patient seems like it has heart disease, so I should be hearing a heart murmur”

A

selective perception

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7
Q

primacy effect

A

initial events in the patient’s medical history or disease are weighted more heavily than events that occur later

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8
Q

what are the 4 clinical reasoning strategies?

A
  1. pattern recognition
  2. arborization
  3. exhaustive search
  4. hypothetical-deductive method
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8
Q

availability heuristic

A

estimating what is more likely by what is most available in your memory: biased towards vivid, unusual, or emotionally charged examples

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9
Q

what are the pros and cons of pattern recognition?

A

pros: quick/efficient, cost-effective, common things look common, quick treatment, life saving!
cons: misdiagnosis, wrong treatment, experience matters, location matters, can lead to rush to judgement, increased morbidity/mortality

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10
Q

what are pros and cons of arborization?

A

pros: unusual differentials, need a pathway to lead to one or other, emergent situations or referrals
cons: doesn’t account for comorbidities, only as good as their designer

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11
Q

what are pros and cons of exhaustive search?

A

pros: rare disease!
cons: overwhelming, often go to as last resort, time consuming, unnecessary diagnoses

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12
Q

what are pros and cons of the hypothetical-deductive method?

A

pros: orderly, kinda ties things together
cons: slow, experience matters

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12
Q

what are the best reasoning strategies?

A

all are used, but best are pattern recognition and hypothetical-deducation

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12
Q

why is the clinical reasoning cycle important?

A

reminds you to be systematic in your approach to cases
self-awareness/metacognition is part of expert reasoning!

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13
Q

what strategy is our model based on?

A

hypothetical-deductive strategy

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13
Q

what clinical reasoning strategy can be summarized as
“it just looks like a case of…”

A

pattern recognition

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14
Q

what clinical reasoning strategy is summarized as “if this is true, then do this…”

A

arborization (decision trees)

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15
Q

what clinical reasoning strategy is basically the bread and butter of vet school?

A

exhaustive search: gather, then sift

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16
Q

why do we care about clinical reasoning strategies?

A

mistakes happen! need to be aware of what you did to lead your decisions. was it a strategy error? a cognitive error? systemic problem?

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17
Q

what are the steps in the clinical reasoning cycle?

A
  1. identify patient
  2. acquire data
  3. summarize data
  4. list problems
  5. generate differentials
  6. justify differentials
  7. identify top differentials
  8. acquire data
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17
Q

how do you organize a case summary (history and PE)

A
  1. signalment and chief complaint
  2. history of current problem
  3. background history
  4. physical exam
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18
Q

what does the liver store glucose as?

A

glycogen

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19
Q

what cells release glucagon?

A

alpha cells of pancreas release glucagon into blood

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20
Q

what breaks down glycogen to release glucose into blood?

A

liver

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21
Q

is insulin anabolic or catabolic?

A

anabolic
increases storage of glucose, fatty acids and amino acids

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22
Q

is glucagon anabolic or catabolic?

A

catabolic
increases mobilization of glucose, fatty acids, and amino acids

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23
Q

what does insulin do to energy production?

A

suppresses it: allows cellular uptake of glucose
suppresses fat lipolysis, fatty acid oxidation, gluconeogenesis, glycogenolysis

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24
Q

without insulin, what happens to the body?

A

hyperglycemia, hyperlipidemia, ketones
no glucose uptake, fatty acid oxidation occurs (ketones), fat lipolysis occurs, gluconeogenesis occurs

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25
Q

history and PE of DM

A

weight loss with polyphagia
PU/PD
cataracts (dogs only)
recurrent infections (UTIs)
hepatomegaly

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26
Q

what species gets cataracts with DM?

A

dogs only

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26
Q

with a dog with weight loss, what do you ask about first?

A

appetite!

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27
Q

what are 3 causes for polyphagia

A
  1. inadequate intake
  2. hypermetabolism
  3. nutrient loss
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28
Q

what are the 4 causes of anorexia

A
  1. primary anorexia
  2. pseudoanorexia
  3. primary GI
  4. secondary GI
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29
Q

what causes PU/PD?

A

osmotic diuresis: glucose is an osmotic agent. water channels are in tubules and water leaves due to the gradient. osmolality of urine is increased

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30
Q

what causes cataracts in dogs with DM?

A

normally, glucose is processed thru anaerobic glycolyic pathway and turned into lactic acid, which readily diffuses out of lens normally
when glucose overwhelms the cells, it goes thru the sorbitol pathway and becomes sorbitol + fructose. it then can’t diffuse out and water builds up in the lens

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31
Q

clinicopathologic changes of DM

A
  • hyperglycemia
  • glucosuria
  • elevated cholesterol
  • elevated liver enzymes
  • minimally concentrated urine
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32
Q

renal thresholds of glucose

A

dogs: 180 mg/dL
cats: 250 mg/dL
once threshold exceeded, you get spillover into urine and thus glucosuria

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33
Q

why do you see elevated cholesterol with DM?

A

lack of insulin = fat metabolism derangement
lipoprotein lipase = impaired: normally clears VLDLs and triglycerides
LDL receptor impaired: clears cholesterol

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33
Q

what are the important mineralocorticoids produced in the adrenal glands?

A

aldosterone, RAAS

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34
Q

what are the important glucocorticoids produced in the adrenal glands?

A

cortisol, ACTH

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35
Q

where are the mineralocorticoids produced?

A

glomerulosa

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36
Q

where are the glucocorticoids produced?

A

fasciculata

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37
Q

what determines production of aldosterone and cortisol?

A

enzymes
aldosterone: aldosterone-synthase
cortisol: 17-a-hydroxylase

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38
Q

what is the 1st step in steroid synthesis?

A

endogenous ACTH stimulation initiates the first step. binding induces cascade of cortisol

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38
Q

what is the axis of stress?

A

hypothalamic-pituitary-adrenal-axis

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39
Q

describe the pathway of the HPAA

A
  1. hypothalamus produces CRH
  2. CRH stimulates the pituitary to produce ACTH
  3. ACTH stimulates the adrenal glands to make cortisol
    negative feedback stops this
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40
Q

what produces CRH?

A

hypothalamus

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41
Q

what produces ACTH?

A

pituitary

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42
Q

describe the consequences of a pituitary tumor

A

pituitary-dependent hyperadrenocorticism
both adrenal glands become hyperplastic. produce tons of cortisol, but there is no suppression to pituitary because the tumor just does its own thing

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43
Q
A
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44
Q

describe the consequences of an adrenal tumor

A

one adrenal gland produces TONS of cortisol, which gives lots of feedback to pituitary telling it to turn off. you get pituitary atrophy.
then get contralateral adrenal gland atrophy due to lack of stimulation

45
Q
A
46
Q

describe consequences of iatrogenic cushing’s

A

suppression of pituitary (ACTH) by exogenous steroids
only the fasciculata atrophy. both adrenal glands atrophy because the pituitary is not stimulating them

47
Q

typical addison’s

A

immune-mediated destruction of BOTH zona fasciculata and zona glomerulosa. thus cortisol AND mineralocorticoids are low

48
Q

in typical addison’s, what is low?

A

cortisol and mineralocorticoids

48
Q

atypical addison’s

A

immune-mediated destruction of ONLY zona fasciculata
only cortisol low

49
Q

in atypical addison’s, what is low?

A

only cortisol is low

50
Q

metabolic effects of cortisol

A
  • floods the body with energy: proteins/glucose/fat to deal with stress
  • maintains blood pressure
  • dampens inflammatory cascade
50
Q

how does cortisol affect energy recruitment?

A
  • increases glucose for energy: gluconeogenesis
  • breaks down protein to feed gluconeogenesis
  • liberates lipids for beta oxidation
51
Q

is cortisol anabolic or catabolic?

A

catabolic! breaks down glycogen, fat, etc. muscle wasting of apaxial muscles typical, get pot belly and redistribution of fat to abdomen and nape of neck
(opposite is hot abs from testosterone)

52
Q

vascular effects of cortisol

A
  • helps maintain vascular response to hypovolemia
  • permissive effect in conjugation with catecholamines
53
Q

what is the vascular effect of a cortisol deficiency?

A

hypotension

54
Q

what is the vascular effect of a cortisol excess?

A

hypertension

54
Q

anti-inflammatory effects of cortisol

A
  • inhibits phospholipase A2
  • prevents formation of important inflammatory products
  • cortisol excess leads to immunosuppression: pyoderma, UTI, etc
55
Q

where are common locations of endocrine alopecia?

A

lateral thorax and abdomen, perineum and caudal thighs
head, neck and extremities spared

55
Q

CNS effects of cortisol

A

polyphagia, polydipsia
cortisol excess and deficiency both cause PU/PD!! but by different mechanisms

56
Q

what is cortisol’s effect on the GI system?

A

maintenance of the GI mucose
cortisol deficiency leads to vomiting and bloody diarrhea

56
Q

what are cortisol’s effects on CBC?

A
  • RBC production, suppresses lymphocytes and eosinophils
  • prevents migration of neutrophils out of circulation
  • see neutrophilia but immunosuppression because the neutrophils can’t get to the site of infection!
57
Q

what CBC abnormalites will you see with a cortisol excess disorder?

A

stress leukogram

58
Q

what CBC abnormalities will you see with cortisol deficiency?

A

lack of stress leukogram and anemia

59
Q

biochemistry abnormalities with a cortisol excess

A
  • increased ALP/GST: steroid-induced isoenzyme and excessive glycogen
  • increased cholesterol: increased lipolysis
  • increased glucose (mild): increased gluconeogenesis
60
Q

biochemistry abnormalities seen with a cortisol deficiency

A
  • increased ALT: shock
  • decreased cholesterol: decreased GI uptake
  • decreased glucose: decreased gluconeogenesis
  • increased K+ and decreased Na : decreased mineralocorticoids
61
Q

urinalysis abnormalities seen with excess cortisol

A
  • decreased USG: ADH inhibition?
  • proteinuria: multifactorial
  • bacteriuria without pyuria: immunosuppression (no evidence of WBC because neutrophils are stuck
62
Q

urinalysis abnormalities seen with a cortisol deficiency

A

decreased USG: decreased mineralocorticoids

63
Q

thyroid hormone ingredients

A
  • iodide trapping mechanism
  • thyroglobulin
  • tyrosine
  • iodine
  • thyroid peroxidase
64
Q

what is thyroglobulin?

A

a protein that creates the string that tyrosine attaches onto

65
Q

what are the steps of making thyroid hormone?

A

organification and synthesis

66
Q

how is thyroid hormone secreted and transported?

A
  • poorly water soluble; uses thyroxine-binding globulin (TBG) to get into cell
  • nearly all >99% of T4/T3 is bound to proteins
  • inactive when bound
67
Q

when is thyroid hormone inactive?

A

when it is bound - nearly all of T4/T3 is bound to proteins

68
Q

thyroid hormone action at the cellular level

A
  • delivered to receptors in the nucleus
  • forms a hormone-receptor complex
  • result: gene transcription or inhibition
69
Q

what is the result of thyroid hormone forming a hormone-receptor complex at the nucleus?

A

gene transcription or inhibition

70
Q

what is the thyroid axis?

A
  1. hypothalamus: TRH: thyrotropin releasing hormone
  2. pituitary gland (anterior): thyroid stimulating hormone (TSH)
  3. thyroid gland: T4 and T3
71
Q

how can thyroid affect growth?

A

disproportionate dwarf: lack of thyroid hormone
proportionate dwarf: lack of growth hormone

72
Q

what are the thyroid effects?

A

growth, development, metabolism, specific systems

73
Q

what is the difference between a disproportionate dwarf and a proportionate dwarf?

A

disproportionate dwarf is a lack of thyroid hormone
proportionate dwarf is a lack of growth hormone

74
Q

how does thyroid hormone affect development?

A

mammals: fetal and neonatal brain development
reptile: metamorphosis won’t occur if frog is deficient in thyroid hormone

75
Q

how does thyroid hormone affect metabolism?

A

increases basal metabolic rate
- stimulates lipolysis
- increases carbohydrate uptake from the gut
- increases gluconeogenesis and glycogenesis
- increases insulin-dependent glucose uptake into cells
- protein catabolism: energy recruitment

76
Q

what cardiovascular effects are seen with a hypothyroid dog?

A

none; rarely clinically significant

76
Q

what cardiovascular effects can be seen with a hyperthyroid cat?

A

hyperthyroidism upregulates the number and affinity of beta-adrenergic receptors
increases cardiac output, leading to tachycardia, +/- arrhythmias, murmurs
hypertension

77
Q

what CNS effects are seen with a hyperthyroid cat?

A

upregulates adrenergic activity? nervousness, hyperactivity, aggression

78
Q

what CNS effects are seen with a hypothyroid dog?

A

mental dullness

79
Q

what PNS effects are seen with a hyperthyroid cat?

A

little clinical significance

80
Q

what PNS effects are seen with a hypothyroid dog?

A
  • demyelination and decreased action potential
    decreased reflexes, forelimb/hindlimb paresis, cranial nerve deficits
81
Q

what skin effects are seen in a hyperthyroid cat?

A

unkempt haircoat

82
Q

what skin effects are seen in a hypothyroid dog? what is the mechanism?

A

hair gets “stuck” in telogen (resting) stage. alopecia in areas of wear, lack of regrowth after clipping, hyperpigmentation

83
Q

what other organs are affected by abnormal thyroid levels?

A

excess thyroid: looking for energy, extra O2 consumption, increased cardiac output, increased renal blood flow. get muscle wasting, fat loss, tachypnea, PU/PD
deficiency in thyroid: weight gain

84
Q

how does thyroid hormone affect CBC?

A

excess: increased O2 consumption in bone marrow, rarely increased PCV
clinically insignificant in both counts

85
Q

what abnormalities are seen on a biochemistry panel of a hyperthyroid cat?

A

liver hypoxia from increased O2 consumption?
- increased gluconeogenesis and protein breakdown leads to increased liver enzymes (ALT > ALP), increased BUN, mild increase in glucose

86
Q

what biochemistry panel abnormalities might you see with a hypothyroid dog?

A

disrupted cholesterol synthesis and degradation: increased cholesterol

87
Q

what abnormalities would you see on a urinalysis of a hyperthyoid patient?

A

increased CO –> increased renal blood flow –> medullary washout: losing fluid
see decreased USG

88
Q

is the parathyroid gland stimulated by increased or decreased calcium?

A

decreased calcium
parathyroid hormone from chief cells
PTH props it up!

89
Q

what abnormalities would you see on a urinalysis of a hypothyoid patient?

A

none

90
Q

is the thyroid gland stimulated by increased or decreased calcium?

A

increased calcium
calcitonin from C cells (parafollicular cells)
calci-tone-in tones it down!

91
Q

how does calcium maintain homeostasis?

A

45-50% protein bound, same amount is ionized (active). 5-10% is complexed with other molecules like phosphate, citrate, bicarb

92
Q

what is the mass law effect?

A

total calcium x total phosphorus = <60
don’t want to exceed 60: will see mineralization of tissues

93
Q

the parathyroid gland gets activated by decreased calcium levels. what does it signal in attempts to raise these?

A
  • bone: increases bone resorption
  • kidneys: increases Ca2+ reabsorption, which increases P excretion, thus decreasing levels of Phosphorus
  • kidneys start producing more vitamin D: which pulls Ca and P in from the GI tract
94
Q

what does vitamin D do in calcium regulation?

A

Vitamin D is produced by the kidneys, it pulls Ca2+ and Phosphorus in from the GI tract

95
Q

what effect does PTH have on Ca2+ and PO4?

A

Ca2+: increases levels
PO4: decreases levels
mass law

96
Q

what effect does calcitonin have on Ca2+ and PO4?

A

decreases both

97
Q

what effect does vitamin D have on Ca2+ and PO4?

A

increases both

98
Q

what are the hypercalcemia rule-outs?

A

GOSHDARNIT
G: granulomatous: fungal
O: osteolytic
S: spurious
H: hyperparathyroidism
D: vitamin D toxicosis
A: addison’s disease
R: renal secondary hyperparathyroidism
N: neoplasia
I: idiopathic
T: toxins

99
Q

granulomatous causes of hypercalcemia

A
  • fungal: blastomycosis and others
  • bone invasion?
  • abnormal vitamin D metabolism by macrophages?
100
Q

osteolytic causes of hypercalcemia

A

osteolytic = tumor
- osteoClast activating factors
- Calcium
- osteosarComa

101
Q

spurious causes of hypercalcemia

A

not real or not abnormal; not pathologic
- lipemia
- hemolysis from sample handling
- hemoconcentration
- hyperalbuminemia : doesn’t actually change iCa2+
- acidosis: favors dissociation of Ca2+ from proteins
- young animal

102
Q

hyperparathyroidism and hypercalcemia

A
  • excessive production of PTH
  • parathyroid adenomas
  • parathyroid hyperplasia
103
Q

vitamin D toxicosis cause of hypercalcemia

A
  • rodenticides: cholecalciferol
  • treatments for psoriasis
  • over supplementation
104
Q

addison’s disease and hypercalcemia

A

usually mild total calcium elevation: iCa2+ usually normal

105
Q

renal secondary hyperparathyroidism and hypercalcemia

A
  • decreased vitamin D production from kidneys
  • phosphorus retention from kidney dysfunction
106
Q

in renal secondary hyperparathyroidism, the kidneys are not functioning properly. they have decreased excretion of phosphorus, which in turn has what effect on calcium? why?

A

decreased excretion of phosphorus means there is increased serum phosphorus, and because of the mass law effect, this increase causes a decrease in serum Ca2+. this will tell the parathyroid gland to increase PTH levels

107
Q

neoplasia and hyperparathyroidism

A

PTH-related proteins: PTHrp: protein that parathyroid gland reads and shuts off. PTHrps take over and increase Ca2+

107
Q

why do you need to be careful with what types of calcium you are measuring?

A

in renal secondary hyperparathyroidism, total calcium is often elevated, but ionized calcium is often normal or decreased. this is what is driving the overproduction of PTH

108
Q

what are the most common tumors causing hypercalcemia?

A

LYMPHOMAAA
apocrine gland adenocarcinomas of the anal sac: AGASACA

109
Q

what species is known for idiopathic hypercalcemia?

A

cats

110
Q

what toxins lead to hypercalcemia?

A
  • plants: day blooming jessamine
  • vitamin D
111
Q

what are clinical signs of hypercalcemia? why?

A
  • PU/PD
  • weakness, listlessness
  • inappetance
  • cardiac arrhythmias
  • calcium oxalate stones
  • UTIs?
    many of these due to decreases in depolarization
112
Q

what are clinical signs of hypocalcemia?

A
  • muscle fasciculation/tetany
  • pruritus/facial rubbing
  • panting
  • nervousness
  • seizures
  • cardiac arrhythmias
    many of these due to rapid depolarization
113
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114
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Clinical Sciences 1 (3 decks)

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