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ACVECC > Renal/end/acid-base > Flashcards

Renal/end/acid-base Flashcards

1
Q

Classification of hormones

A
  1. Protein/peptide: ACTH, CRH, insulin
    - Synthesized as prehormones
    - Composed of amino acids
    - Receptors on cell membrane
  2. Steroid Hormone (aldosterone, cortisole)
    - Synthesized from cortisol
    - Lipid soluble
    - Receptors in cytoplasm
  3. Tyrosine Derived Hormones
    - Catecholamines & thyroid hormones
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2
Q

2 phases of liver metabolism

A

Phase I: Hydroxylation/oxidation
Phase II: Glycuronidation/sulfation

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3
Q

Intracellular signaling with G coupled protein receptors

A

Adenyl CYclase –>cAMP–> PKA & phosphorylation of proteins

Phospholipase C –> IP3/DA –> protein kinase C resulting in phosphorylation IP3 –> increased intracellular calcium

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4
Q

Hypothalamus Control of pituitary

A

Anterior: neuroendocrine control of anterior pituitary

Posterior: Release neuropeptides in hypothalamic neurons

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5
Q

ADH secretion

A

Increased with: hypovolemia, decreased BP, nausea, pain, stress, barbiturates, morphine, nicotine, pther drugs

Decreased with: hypervolemia, hypertension, alcohol

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6
Q

What neuropeptides synthesized in parvocellular neurons

A

Anterior hypothalamus –> anterior pituitary

  • CRH
  • TRH
  • GnRH
  • GHRH (growth)
  • Dopamine
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7
Q

Hormones from posterior pituitary

A

ADH
Oxytocin

Via magnocellular neurons

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8
Q

Different aquaporin receptors

A

AQP1: 90% receptors
- Luminal surface of thin LOH & proximal tubules

AQP2: only one that requires ADH - collecting duct

AQP 3& 4: basolateral membrane

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9
Q

Body management of oamolality

A
  • Changed osmotic pressure sensed by hypothalamus osmoreceptors: subfornical organ, median preoptic nucleus & OVLT
  • INcreased osmol –> cells shrink –> ADH release
  • Decreased osmol –> cell swelling -> decreased ADH

*Sensitive to 1-2% change in osmolality

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10
Q

Biologic effects of thyroid hormones

A
  • Receptors in all tissues

CV: inotropic/chronotropic
Bone: Growth
Liver: cholesterol metabolism

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11
Q

Calcium functions

A
  • Coagulation
  • Intracellular signaling
  • 2nd messenger system
  • action potential generation
  • Neuronal transmission
  • Bone structure
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12
Q

What factors control PTH release

A
  • Calcium
  • Phosphorus
  • Magnesium
  • Vitamin D
  • Beta stimulation (increased PTH)
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13
Q

Renal effects of PTH

A
  • Increased insertion of calcium channels on apical membranes of distal tubules
  • increased calbindin –> facilitates diffusion into cell
  • Increased calcium movement through basolateral membrane (calcium ATPase & Na-Ca exchange)
  • Increased 1alpha hydrolase –> activates vitamin D
  • Decreased Na-PO4 cotransporter at proximal tubule
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14
Q

PTH effect on bone

A
  • Extracellular matrix
  • Osteoblasts express PTH receptor –> increase proliferation
  • Activation of osteoclasts:ruffled border in folding plasma membrane

Resorbs bone

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15
Q

3 fractions of calcium

A

50% iCa
40% protein bound
10% complexed

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16
Q

Cellular effects of vitamin D

A
  • Bind cellular steroid receptors in target tissue

Target Tissue: Bone, kidney, intestines

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17
Q

Function of calcitonin

A
  • Decreases Calcium!!

-Decreases bone resorption
-Inhibit osteoclasts
-Increase calcium excretion

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18
Q

Zona glomerulosa

A
  • outer most layer
  • Lacks 17alpha hydroxylase
  • Aldosterone synthesis!!
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19
Q

Metabolism of glucocorticoids

A
  1. Lipophilic –bound to carrier proteins
    - Transcortin
    - Albumin
    - Cortisol bindling globulin
  2. Diffuse intracellularly binding to cytosolic receptors
  3. Elimination:
    - Liver: biotransformation - conjugation –> excretion
    - Localized tissue metabolism
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20
Q

Describe synthesis release of mineralocorticoids

A
  1. Synthesis & release regulated by:
    - AngioII
    - RAAS stimulation
    - ACTH
    - Hyperkalemia
  2. Metabolism
    - Liver/renal excretion

Made from cholesterol

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21
Q

Functions/effects of mineralocorticoids

A
  1. Regulate Na/K/H2O
  2. Receptors in distal tubule/collecting duct
    - Principal cells
    - inc transepithelial Na
    - Inc apical Na channels
    - Inc basolateral Na/K ATPase
    - Inc H-ATPase (inc H excretion)
    - Inc HCO3-Cl exchange
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22
Q

Adrenal medulla

A
  • SNS ganglion
  • Release of Ach bind chromaffin cells–> catecholamine release

**Very vascular

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23
Q

Catecholamine degraded by

A

COMT & MAO

**Break down into metanepherine and normetanephrine

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24
Q

Alpha and Beta effects

A

Alpha: Vasoconstriction, bladder sphincter contraction, bronchoconstriction, increased hepatic glucose production, decreased insulin, cardiac contractility, iris dilation, intestinal relaxation, pilomotor contraction

Beta: vasodilation, bladder relax, bronchodilation, glycogenolysis, increased glucagon, increased inotropy, lipolysis, increased renin

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25
Q

Pathophysiology hepatic encephalopathy

A

Inc NH3 + inc BBB permeability –> NH3 decreases excitatory neurotransmitters (NMDA, Cl postynapsis)

NH3 removed by transamination of glutamate into glutamine in astrocytes –> Glutamine exchange across BBB for tryptophan, serotonin & quinolate AND glutamine converted to glutamate –> overstimulated NMDA receptors

-Increases GABA tone–> due to increased NH4 & Mg –> inc peripheral type benzo receptors –> increased synthesis neuro steroids–> act on GABA

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26
Q

Granulomatous liver infections

A

Mycobacteria
Leishmania
Bartonella
Migrating nematodes

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27
Q

Biliary parasites

A

Platynosum concinnum
Amphimerus pseudofelineus

TX praziquantal

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28
Q

DDX infectious chronic hepatitis

A

RIckettsia
Salmonella Sp
Clostridium Sp
Campylobacter jejuni
Yersinia pseudotuberculosis

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29
Q

DDX acute hepatitis in dogs

A

Infectious: CAV-1 (adenovirus), lepto, clostridium, E.canis, herpes

Drugs: carprofen, acetaminophen, TMS, azathioprine, amioderone, mitotane

Idiopathic

Toxin: mycotoxin, cyanobacteria (blue-green algea), amanita, xylitol, alpha lipoic acid (human OTC antioxi), organic solvents (CCl4 - kill insects in grain)

30
Q

MC biliary infections

A

Bacteriodes
Streptococcus
E.coli – emphysema may be present
Enterococcus
Clostridium - emphysema may be present
Helicobacter canis

31
Q

Decrease phosphorus and RBC

A

Decreased CO2 –> shift of CO2 from intracellular to extracellular space –> increased intracellular pH –> increased use phosphate to phosphorylate glu –> RBC hemolysis

32
Q

Tryptophan MOA in hepatic encephalopathy

A
  • Directly neurotoxic
  • increased serotonin: NMDA inhibition
  • Increased Quinolic acid: NMDA excitation
33
Q

Mechanism of Hepatic enceph NH4

A
  • NH3 transamination to glutamine in astrocytes –> increases tryptophan in brain
  • Inc excitability (over stimulate NMDA with help of glutamine)
  • Dec excitability (inhibits Cl- extrusion from post synaptic cell; down regulate NMDA receptors)
  • Brain edema
  • Decreased microsomal Na/K ATPase in brain
34
Q

Short chain fatty acids & hepatic encephalopathy MOAs

A
  • Displaces tryptophan from albumin–> increase free tryptophan
35
Q

GABA MOA in hepatic encephalopathy

A
  • unclear if increased GABnergic tone
  • NH3 & Mg increase expression of peripheral type benzo receptors
  • increased neurosteroids bind and increase GABA activity peripherally
36
Q

Glutamine MOA hepatic encephalopathy

A
  • Alters BBB amino acid transport: Increased Trypotophan exchange –> increases serotonin and quinolate in brain
  • Glutamine transported from astrocytes to neurons –> convert to glutamate–> overstimulates NMDA receptors (increased excitation)
  • May cause increased osmolality of neurons –> cell swelling
37
Q

Excess compounds with HE

A
  • NH4: increased glutamine -
  • Endogenous benzos receptors
  • Neurosteroids
  • Glutamine
  • Aromatic amino acids
  • Short chain fatty acids (inc tryptophan)
  • Tryptophan
  • Increased manganese
38
Q

FAlse neurotranmitters in Hep Enceph & MOA

A
  • Tyrosine –> Octapamine
  • Phenylalanine –> phenylethylamine
  • Methionine –> mercaptans
  • inhibit/impair NE action
  • Synergistic with NH4 & SCFA
  • Dec NH4 detox in brain urea cycle
  • Dec microsomal Na/K ATPase
39
Q

MOA HE aromatic amino acids

A
  • Normally balanced by nonaromatic AA
  • Leads to increased production of false neurotransmitters & decreased dopamine & norepinephrine –> coma
40
Q

MC bacteria pyometra

A
  • MC ecoli

-strep
-enterobacter
-proteus
-klebsiella
-pseudomonas

41
Q

4 phases AKI

A
  1. Initiation: subcellular injury
  2. Extension: cellular injury –> death –> biochemical derangements & clinical manifestation of disease
  3. maintenance: Cell death & regeneration simultaneously –> poss recovery determined by balance between 2
  4. Recovery: Improved GFR & tubular function ** may last weeks to months**
42
Q

UOP categories

A

Anuric - none
Oliguric (<0.5 ml/kg/hr)
polyuric (>2 ml/kg/hr)

** Fluid overload >10% baseline body weight

43
Q

Causes of Resp Acidosis

A

** Increased CO2 production or decreased minute ventilation**
-Pulm/small airway disease
- Resp center depression
- NM disease
- Restrictive extrapulmonary disorders
- Large Airway obstruction
- Marked Obesity
- Ineffective mechanical ventilation
- INc CO2 product( hyperthermia, seizures, fever, malignant hyperthermia)

44
Q

Causes of respiratory alkalosis

A
  • Iatrogenic (mechanical vent)
  • Hypoxemia –> stim increased minute ventilation
  • Severe Pulmonary disease
  • centrally mediated hyperventilation
  • Pain, fear, anxiety
45
Q

Normochloremic metabolic acidosis

A
  • has increased anion gap (may be inapp elevated if hyperalbuminemia)
  • DUEL
  • DKA
  • Uremia
  • Ethylene glycol
  • Lactic acidosis
  • Other/less common:
    D-lactic acidosis
    Salicylate ingestion
    methanol intoxication
46
Q

Expected compensatory changes in met acidosis

A

Met acidosis
- dec pCO2 0.7 mmHG –> 1 mEq/L dec in [HCO3] +/-3

Met alkalosis
- Inc pCO2 of 0.7 mmhg –> 1 mEq/L decrease in HCO3 +/- 3

47
Q

Causes of metabolic alkalosis

A

Cl responsive
- vomiting
- diuretics
- correction of resp acidosis

Cl resistant
- primary hyperaldosteronism
- Cushings
- Over administration of alkaline fluids

48
Q

Hyperchloremic metabolic acidosis causes

A
  • GI loss –> loss Na relative to Cl (bicarb loss)
  • Renal bicarb loss
  • Hypoadrenocorticism
  • NaCl adminmistration
  • Renal tubular acidosis
49
Q

Oliguria

A

UOP less than noraml ( dogs <0.27 ml/kf/hr)

  • Hydrated, well perfused pt: <1 ml/kg/hr = absolute oliguria
  • Pt with IVF UOP 1-2 ml/kg/hr = relative oliguria
  • Prerenal oliguria: urine [Na] <20 mEq/L
50
Q

Prerenal causes polyuria

A
  • increased intake : psychogenic OD, IVF
  • Drugs: diuretics, alpha2 agonists, K agonist, alcohols, steroids, anticonvulsents
  • Hormonal: hyper/poadrenocortiscism, diabetes insipidis, increased T4, cerebral salt wasting syndrome
  • Electrolytes: low K, HIgh Ca
  • Osmotic: diabetes, salt ingestion, glycols, e.coli endotoxin, liver disease
51
Q

Postrenal polyuria

A

Post obstructive diuresis

  • Likely due to proximal tubule dysfunction, altered ADH responsiveness & osmotic diuresis

**Tx aggressive IVF

52
Q

Insensible losses

A

Cannot be measured

-Evaporation can be 20-70 ml/kg/day depending on activity of patient

53
Q

Catheter assd bactiuria

A

Asceptically obtained urine from indwelling catheter within 48 hrs of removal of cath that tests + for species of bacteria at 10^5 CFU/ml

54
Q

Body’s processes to maintain acid base

A
  1. regulation PCO2 by ventilation
  2. Buffering of acids with bicarb, PO4, and proteins
  3. Changes in renal excretion of acid or base
55
Q

2 mechanisms metabolic acidosis

A
  1. Bicarb loss(Cl- gain)
    - GI loss
    - renal loss –> appropriate response or renal tubular acidosis
    - Admin NaCl

2.Acid gain
- DUEL
-Salicylate ingestion (aspirin)
- methanol intoxication

56
Q

4 mechanisms extracorporeal therapy

A
  1. diffusion –> small & some medium MW solutes move easily. Charges have some effect (dialysate has physiologic levels of things (Na, glu, k, ect )in plasma )
  2. Convection–>Flow of solutes by hydrostatic or osmotic gradients (water drags solutes with it)
    - Removal small medium and large MW solutes
  3. Ultrafiltration –> removing fluid (WATER) from blood via hydrostatic pressure (For FO)
  4. Adsorption: sticking to membrane (toxins, not huge thing in renal cases)
57
Q

RAAS

A
  • Decreased renal blood Q & Na to distal tubule → macula densa releases renin→ Renin converts Angiotensinogen (from liver) to Angiotensin I→ ACE converts Angio I to Angio II → aldosterone production→ renal Na and water retention, myocardial apoptosis, cardiac and vascular remodeling & fibrosis, increased thirst and vasoconstriction
  • Local tissue RAAS is thought to encourage local cardiac remodeling
  • Angio II can be generated from pathways independent of ACE → therefore can still have aldosterone and Angio II production with ACE inhibitors
  • Aldosterone
58
Q

What causes an increase in anion gap?

A

Ketones, lactate, uremia, methanol, ethylene glycol, metaldehyde

  • Only reason for low AG is albumin low
    Not useful in hypoalbuminemia
59
Q

Renal Tubular Acidosis
Distal

A

Distal: Urine cannot be maximally acidified due to impaired H+ ion secretion in the collecting ducts
urine pH >6.0 despite markedly decreased plasma [HCO3]

Step 1: rule out ureases positive UTI ( Proteus sp., Staphylococcus aureus)

Step 2: Diagnosis is confirmed via ammonium chloride tolerance test during which urine pH is monitored before and after at hourly intervals for 5 hours after oral administration of 0.2 g/kg NH4Cl

Treatment potassium citrate

Often companied by hypOkalemia

  • Causes: pyelonephritis, IMHA, addisons
60
Q

Renal tubular Acidosis Proximal

A

Proximal: Renal reabsorption of HCO3 markedly reduced and urinary fractional excretion of HCO3 is increased (>15%) when HCO3 is increased to normal

  • Diagnosis: acidic urine pH <5.5 or 6 in the presence of hyperchloremic metabolic acidosis and a normal GFR BUT after plasma HCO3 is normalized by akali administration, an increased urine pH (>6.0) and increased urinary fractional excretion of HCO3 (>15%)
  • Next Step: Rule out Fanconi (add prox tubular dysfunction): glucouria despite normal BG
  • Difficult to correct. As normalize blood HCO3, they excrete more
  • Causes: fanconi syndrome, toxins, drugs, hypoparathyroidism, multiple myeloma
61
Q

Adverse effects of metabolic acidosis

A
  • Decreased myocardial contractility,
  • Arterial vasodilation & venoconstriction
  • Impaired coagulation
  • increased work of breathing secondary to CO2 production
  • Decreased renal and hepatic blood flow
  • insulin resistance
  • Altered central nervous function
62
Q

Indications for Dialysis

A
  • severe progressive azotemia (Crea >10 or anuria)
  • Severe hyperkalemia NOT responding to medical management
  • Life threatening FO (esp if oliguric or anuric)
  • Severe acid base disturbances
  • Uncontrolled uremia that is unresponsive or minimally responsive to traditional medical management (after 12-24 hours on IVF)
63
Q

Contraindications Dialysis

A

Hemodialysis
- coagulopathy - especially when only heparin is availble and not regional citrate
- Severe hypotension

Peritoneal dialysis
- peritonitis
- recent abdominal or thoracic surgery
- Hypoalbuminemia
- Severe hypercatabolic states

64
Q

Different extracoporeal types (intoxications)

A
  1. Hemofiltration: works by diffusion –> effective with small (<500-1000Da), water soluble solutes with low protein binding (<80%)
  2. Hemofeiltratoin/hemodiafiltration: works by convection; better for larger solutes (1000-10x Da)
  3. Hemoperfusion: works via adsorption; large particles (>10K da) or with high protein binding (>95%)
  4. Plasmapharesis: works via centrifugation; good for large (>50x Da) or highly protein bound (>95%) that are in plasma compartment
65
Q

Causes of acquired CENTRAL diabetes insipidis

A
  • Brain trauma
  • Neoplasia (intracranial or lymphoma)
  • INfectious/inflamm (meningitis, encephalitis, toxo, histiocytosis, crypto)
  • Vascular (hypothalmic infarction, intracranial hemorrhage or hypoxic enceph)
  • Immune mediated
  • Idiopathic
66
Q

Causes of acquired NEPHROGENIC diabetes insipidis

A
  • Drugs (vasopressin, ofloxcin, ampho B, aminoglycosides, cisplatin, vinblastine, colchicine)
  • Electrolyte abnormalities (hypercalcemia, hypokalemia)
  • Bacteria (E. Coli, Streptococcus, lepto) –> pyo, pyelo, SEPSIS
  • Degenerative (CKD, amyloidosis)
  • Paraneoplastic (Intestinal leiomyosarcoma)
  • Addisons
  • Liver insufficiency/ PSS
67
Q

Causes SI ADH

A
  1. CNS disease
    - bleeding mass or lesion (hydrocephalus)
    - infection (meningitis)
    - Other (TBI in human, liver disease)
  2. Pulmonary Disease
    - Pneumonia
    - PPV in humans
  3. Drugs
    - Vinca alkaloids
    human med:
    - PPIs
    - SSRIs
    - Opiates
  4. Idiopathic
  5. Immune mediated Disease
68
Q

Diagnostic Criteria of SI ADH

A
  1. hypoosmolar hyponatremia*
  2. euvolemia
  3. Inappropriately concentrated urine (U osm >100 mOsm/L)*
  4. Urine Na concentration >30 mmol/L
  5. Hypoadrenocorticism excluded
  • *If not able to check immediate osmolality : USG >1014 expected, but USG >1005 suggestive of Uosm >100**
69
Q

Clinical signs of thyroid storm

A
  • CNS disturbances (msot commn in feline pts)
  • HypERthermia (often not present in felines)
  • Acute vomiting or diarrhea
  • Abdominal pain
  • Extreme muscle weakness & cervical ventroflexion
  • Icterus
  • Cardiac murmurs +/- arrhythmias
  • Pleural effusion
  • Pulmonary edema
  • Tachypnea
  • Hypertension
  • Retinopathies
  • Thromboembolic disease
  • Sudden death

** Human Med muhave 4 major signs:
1. CNS signs
2. GI and hepatic dysfunction
3. Fever
4. Cardiovasc signs**

70
Q

Drugs to avoid with pheochromocytoma

A
  • Metoclopramide
  • Histamine
  • Tyramine
  • Glucagon
  • Anticholinergics –> preop avoid (ace, atropine), inc SNS
  • Barbituates –> vent arrhyth, inc SNS
  • Halothane - sensitizes myocardium to catecholamines
  • Long acting beta blockers –> loss B2 vasodilation may worsen hypertension
71
Q

Hepatorenal Syndrome

A

Rare in VM

72
Q

Diagnosis DI

A

Consider if:
- USG 1001-1007 (complete)
- USG 1015-1018 (Partial)

Diagnosis requires:
- rule out of toher diseases
- Measurement water consumption (>100 ml/kg/day), measurement UOP (>50 ml/kg/day) & USG </= 1012
- Normal UA/u culture
- AUS, XR
- IF all above normal, modified water deprivatoin test (must r/o psychogenic or primary polydypsea)

ACVECC (10 decks)

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