3rd exam Flashcards

1
Q

functional unit of the kidney

A

 Nephron:

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2
Q

extend deep into the medulla and are important for the concentration of urine

A

 Juxtamedullary nephrons

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3
Q

The name of the glomerulus and bowman capsule together

A

 Renal Corpuscle

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4
Q

lie between and support the capillaries; have phagocytic ability similar to monocytes, release inflammatory cytokines, and can contract to regulate glomerular capillary blood flow

A

 Mesangial Cells

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5
Q

are covered with protein molecules bearing anionic (negative) charges that retard the filtration of anionic proteins and prevent proteinuria

A

 The endothelium, basement membrane, and podocytes

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6
Q

sodium-sensing cells of the distal tubule

A

 Macula densa

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7
Q

renin-releasing cells; located around the afferent arteriole where it enters the glomerulus

A

 Juxtaglomerular cells

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8
Q

network of capillaries forms loops and closely follows the loops of henle; is ONLY blood supply to the medulla

A

 Vasa Recta

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9
Q

smooth triangular area between the openings of the two ureters and the urethra

A

 Trigone:

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10
Q

directly related to the perfusion pressure of the glomerular capillaries

A

 GFR

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11
Q

receive about 20% to 25% of the cardiac output

A

 Kidneys

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12
Q

 Renin release is stimulated by

A

decreased blood pressure in the afferent arterioles, which reduces the stretch of the juxtaglomerular cells, decreased sodium chloride concentration in the distal convoluted tubule

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13
Q

when the carrier molecules for glucose become saturated (hyperglycemia) the excess will be excreted in the urine

A

 Transport Maximum

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14
Q

function is to actively reabsorb sodium

A

 Proximal tubule

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15
Q

occurs in loop of Henle, distal tubules, and collecting ducts

A

 Urine concentration or dilution

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16
Q

receives fluid from the proximal tubule; highly permeable to water but it is the only place in the nephron that does not actively transport either sodium or chloride; H2O reabsorbed and NaCl and urea diffuse in

A

 Descending limb of the loop

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17
Q

: to water; water cannot follow the sodium-chloride transport; causes the ascending tubular fluid to become hypoosmotic and the medullary interstitium to become hyperosmotic impermeable; tight junction water impermeable; NaCl actively reabsorbed

A

 Ascending limb of the loop

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18
Q

straight segment of the distal tubule and the collecting duct are permeable to water as controlled by ADH; a cause of oliguria (diminished excretion of urine)

A

 ADH:

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19
Q

stimulates the epithelial cells of the distal tubule and collecting duct to reabsorb sodium (promoting water reabsorption) and increases the excretion of potassium and hydrogen ion

A

 Aldosterone

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20
Q

any agent that enhances the flow of urine; interfere with renal sodium reabsorption and reduce extracellular fluid volume; used to treat hypertension and edema caused by heart failure, cirrhosis, and nephrotic syndrome

A

 Diuretic

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21
Q

 Common side effects

 Diuretic

A

hypokalemia, dehydration

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22
Q

(necessary for the absorption of calcium and phosphate by the small intestine)

A

 Kidneys activate vitamin D

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23
Q

 Erythropoietin

A

stimulates the bone marrow to produce RBC in response to tissue hypoxia; stimulated by decreased oxygen delivery to the kidneys

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24
Q

: provides best estimate of functioning renal tissue

A

 GFR

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25
Q

and plasma creatinine concentration are inversely related

A

 GFR

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26
Q

dilation of the renal pelvis and calyces proximal to a blockage leads to ________; enlargement of the renal pelvis and calyces

A

 Hydronephrosis:

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27
Q

cause unobstructed kidney to increase the size of individual glomeruli and tubules but not the total number of functioning nephrons

A

 Compensatory hypertrophy and hyperfunction

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28
Q

(stones): common urinary cause of urinary tract obstruction

A

 Calculi

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29
Q

stones: most common

A

 Calcium

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30
Q

described as moderate to severe pain often originating in the flank and radiating to the groin, usually indicates obstruction of the renal pelvis or proximal ureter

A

 Renal colic

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31
Q

 Lower Urinary Tract Obstruction (2)

A

 Lower Urinary Tract Obstruction
 Detrusor hyperreflexia
 Stress incontinence

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32
Q

neurologic disorders that develop above the pontine

A

 Detrusor hyperreflexia

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33
Q

 Stress incontinence: involuntary loss of urine during coughing, sneezing, laughing, or other physical activity associated with increased abdominal pressure

A

 Stress incontinence

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34
Q

 Complicated UTI (4)

A
	Complicated UTI
	Escherichia coli
	Cloudy urine
	Pyelonephritis
•	Risk factors: urinary obstruction and reflux of urine from the bladder (vesicoureteral reflux)
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35
Q

: develops when there is an abnormality in the urinary system or a health problem that compromises host defenses or response to treatment; pyelonephritis, prostatitis or kidney stones

A

 Complicated UTI

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36
Q

most common infecting microorganism

A

 Escherichia coli

uti

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37
Q

: an infection of one or both upper urinary tracts (ureter, pelvis, and interstitium

A

 Pyelonephritis

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38
Q

• Risk factors: UTI

A

: urinary obstruction and reflux of urine from the bladder (vesicoureteral reflux

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39
Q

: inflammation of the glomerulus

A

 Glomerulonephritis:

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40
Q

• Most common type: (acute postinfectious glomerulonephritis)

A

Streptococcus

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41
Q

-antibody complexes; caused by deposition either of circulating antibodies or of antibodies formed in situ to antigens

A

• Membranous glomerulonephritis

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42
Q

anti-glomerular basement membrane disease; associated with antibody formation against both pulmonary capillary and glomerular basement membrane

A

• Goodpasture syndrome:

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43
Q

excretion of 3.5 g or more of protein in the urine per day and is characteristic of glomerular injury

A

 Nephrotic syndrome:

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44
Q

• Disturbances in the glomerular basement membrane and podocyte injury lead to increased permeability to protein and loss of electrical negative charge

A

Nephrotic syndrome:

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45
Q

• Hypoalbuminemia;

A

proteinuria; edema; hyperlipidemia results

Nephrotic syndrome:

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46
Q

: sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood as demonstrated by an elevation in plasma creatinine and blood urea nitrogen levels

A

 Acute Kidney Injury

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47
Q

associated with hypertension, diabetes mellitus, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies

A

 Chronic Kidney Injury:

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48
Q

systemic symptoms associated with the accumulation of nitrogenous wastes and accumulation of toxins in the plasma caused by the decline in renal function

A

 Uremia

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49
Q

(increased risk of fractures)

A

 Hypocalcemia

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50
Q

decreases red blood cell production and uremia decreases red blood cell life span

A

 Inadequate production of erythropoietin

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51
Q

scratching due to uremic skin residues

A

 Pruritus

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52
Q

a buildup of metabolic waste products occurs when

A

 When the kidneys do not function efficiently

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53
Q

must be excreted daily to prevent toxicity or “hyper” states include, potassium, hydrogen ions and acids

A

 Electrolytes that must be excreted

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54
Q

): the main regulator of the circulating platelet mass; induces platelet production in the bone marrow; platelets express receptors for TPO

A

 Thrombopoietin (TPO):

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55
Q

site of fetal hematopoiesis (blood cell production)

A

 Spleen:

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56
Q

colony-stimulating factors (hematopoietic growth factors); stimulate the proliferation of progenitor cells

A

 Several cytokines participate in hematopoiesis

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57
Q

produced by the kidneys; hormone that stimulates erythrocyte production
 In conditions of tissue hypoxia, erythropoietin is secreted by the kidney

A

 Erythropoietin

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58
Q

Fe3+ hemoglobin that cannot bind to oxygen

A

 Methemoglobin:

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59
Q

% of total body iron is bound to heme in erythrocytes (hemoglobin)

A

 67% of

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60
Q

transports iron within the blood; glycoprotein synthesized primarily by the liver but also by tissue macrophages

A

 Transferrin:

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61
Q

: Breakdown of blood clots

A

 Fibrinolysis

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62
Q

digests the fibrin into smaller soluble pieces (fibrin degradation products)

A

 Plasmin

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63
Q

an enzyme that dissolves clots (fibrinolysis) by degrading fibrin and fibrinogen into FDPs

A

 Plasmin

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64
Q

leukocytosis (high levels of circulating leukocytes) often occurs after

A

 Splenectomy:

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65
Q

: most abundant cell in the blood

A

 Erythrocytes

66
Q

most abundant leukocyte; chief phagocyte in early inflammation

A

 Neutrophils:

67
Q

: neutrophil, eosinophils, basophils

A

 Granulocytes:

68
Q

have cytoplasmic granules that contain vasoactive amines (histamine) and anticoagulant (heparin)

A

 Basophils

69
Q

attacks parasites and fungi

A

attacks parasites and fungi Eosinophil

70
Q

increased eosinophils due to infections

A

• Eosinophilia

71
Q

• Most common mechanism is via the parasitic route

A

• Eosinophilia

72
Q

monocytes, macrophages, lymphocytes, NK cells

A

 Agranulocytes:

73
Q

: contain cytoplasmic granules capable of releasing proinflammatory biochemical mediators when stimulated by injury to a blood vessel

A

 Platelets:

74
Q

is necessary for many of the intracellular signaling mechanisms that control platelet activation

A

 Calcium

75
Q

they are unable to aggregate- a platelet plug cannot be formed with insufficient aggregation

A

 When platelets degranulate

76
Q

blood flow slows down thus leading to decreased oxygen supply to organs (ischemia)

A

 Polycythemia Vera: excessive RBCs

77
Q

 Polycythemia Vera treatment

A

blood transfusions (phlebotomy)

78
Q

 Symptoms: Cerebral thrombosis, viscous blood, chest pain; painful itching

A

 Polycythemia Vera:

79
Q

 Prognosis: Acute myeloid leukemia (AML), occurring spontaneously in 10% of individuals and generally being resistant to conventional therapy

A

 Polycythemia Vera:

80
Q

 Primary cause: Epstein-Barr virus
 Recovery time: 3 weeks
 Symptoms: fatigue, sore throat, fever, lymph node swelling, spleen enlargement

A

 Mononucleosis: kissing disease

81
Q

malignant disorder of the blood and blood forming organs; WBC cancer
 Most common is children

A

 Leukemia

82
Q

: malignant tumor of the bone marrow; malignant plasma cells that infiltrate bone marrow and aggregate into tumor masses throughout the skeletal system
 Cancer of the plasma cells (B cells- neutrophils, monocytes, basophils, eosinophils)

A

 Multiple Myeloma

83
Q

: occurs as myeloma cells replace oxygen carrying RBCs in your bone marrow

A

 Anemia:  Multiple Myeloma

84
Q

: hypercalcemia; renal injury (M protein); anemia; Bone lesions (lytic- break down of bone)

A

 Multiple Myeloma

 End organ damage:

85
Q

 General cause of cancer:

A

SMOKING

86
Q

characterized by enlarged lymphnodes; proliferation of lymphocytes and monocytes

A

 Lymphadenopathy

87
Q

progression from one group of lymph nodes to another

 Presence of Reed-Sternberg (RS) cells

A

 Hodgkin Lymphoma

88
Q

 Symptoms: intermittent fever, drenching night sweats, itchy skin (pruritus), and fatigue

A

 Hodgkin Lymphoma

89
Q

(DIC): an acquired clinical syndrome characterized by widespread activation of coagulation, resulting in formation of fibrin clots in medium and small vessels throughout the body

A

 Disseminated intravascular coagulation

90
Q

 Results from a “consumption of clotting factors”

A

 Disseminated intravascular coagulation (DIC):

91
Q

 Insufficient factors available to complete the extrinsic and intrinsic coagulation cascades resulting in “microvascular bleeding” that can be life threatening

A

Disseminated intravascular coagulation (DIC):

92
Q

 Causes: Human Papillomavirus (HPV) infection

A

 Cervical cancer:

93
Q

 Stages of cancer (overall):

A

 (1) Growth limited to tissue of origin (localized)- easiest to treat
 (2) Cancer is still local but invasive to neighboring tissues
 (3) Cancer spreads to lymph nodes
 (4) Distant metastases; spreads to distant organs- most invasive

94
Q

 Mainly stored in liver (20 years worth of B12)
 Nasty coded tongue; nerve damage if not correct
 Dark green leafy vegetables contain B12

A

 B12 Deficiency: problem is pregnancy

95
Q

 Certain cancers are more likely to occur when

A

when a chronic disease is present

96
Q

increase the risk of developing colon cancer

A

 Chrohn’s disease and ulcerative colitis increase

97
Q

 In males, without GnRH, —- cannot be secreted

A

FSH

98
Q

secretion from the anterior is stimulated by TRH from the hypothalamus and by decreased serum levels of T4 and T3. Secretion of TSH stimulates the synthesis and secretion of thyroid hormones.

A

 Thyroid-stimulating hormone (TSH)

99
Q

 Water soluble homones:

A

protein homrones

100
Q

 Circulate throughout the body in unbound form

A

 Water soluble homones: protein homrones

101
Q

 Act as first messengers, binding to receptors on the cell’s plasma membrane

A

 Water soluble homones: protein homrones

102
Q

 The signals initiated by hormone-receptor binding are then transmitted into the cell by the action of second messengers

A

 Water soluble homones: protein homrones

103
Q

Thyroid hormones and steroids (cortisol):

A

 Lipid-soluble hormones

104
Q

 Circulate throughout the body bound to carrier proteins

A

 Lipid-soluble hormones

105
Q

 Cross the plasma membrane by diffusion

A

 Lipid-soluble hormones

106
Q

 Diffuse directly into the cell nucleus and bind to nuclear receptors

A

 Lipid-soluble hormones

107
Q

low concentrations of hormone increase the number of receptors per cell

A

 Up-regulation

108
Q

: high concentrations of a hormone decrease the number of receptors

A

 Down-regulation

109
Q

 Anterior pituitary: produces (6)

A

GH, ACTH, TSH, FSH, LH, prolactin

110
Q

 Posterior pituitary: produces (2)

A

ADH, oxytocin

111
Q

ACTH regulates (check)

A

the release of cortisol from the adrenal cortex

112
Q

regulates the activity of the thyroid glad

A

• TSH:

113
Q

causes uterine contraction and lactation in women and may have a role in sperm motility

A

• Oxytocin

114
Q

• Functions near the end of labor to enhance effectiveness of contractions, promote delivery of the placenta, and stimulate postpartum uterine contractions, thereby preventing excessive bleeding

A

Oxytocin

115
Q

: increased water reabsorption

A

• ADH

116
Q

• Secretion regulation: osmorecptors of the hypothalamus; as plasma osmolality increases these osmorecptors are stimulated, the rate of ADH secretion increases, more water is reabsorbed from the kidney

A

ADH

117
Q

: insufficient activity of ADH leading to polyuria

A

 Diabetes insipidus:

118
Q
  • Excessive thirst and excretion of large amounts of severely diluted urine
  • Similar to untreated diabetes mellitus except does NOT contain glucose
  • Can develop into large bladder capacity and hydronephrosis
A

Diabetes insipidus:

119
Q

lowers serum calcium levels by inhibition of bone-resorbing osteoclasts

A

 Thyroid: Calcitonin

120
Q

• Secretion is regulated by TRH through negative feedback loop that involves the anterior pituitary and hypothalamus

A

 TH:

121
Q

: necessary for TH synthesis

A

• Iodine:

122
Q

): glycoprotein that is the precursor of TH; combines with iodine

A

• Thyroglobulin (TG):

123
Q

transports TH within the blood

A

• Thyroxine-binding globulin (TBG

124
Q

• Secretion of T3 and T4 controlled by

A

TSH

125
Q

• Physiologic Function: metabolic rates of all cells; causes synthesis of enzymes, proteins and other substances

A

 TH:

126
Q

• Secretion is regulated by TRH through negative feedback loop that involves the anterior pituitary and hypothalamus

A

 TH:

127
Q

can cause mental retardation and stunts physical growth

A

 Congenital Hypo and Hyperthyroidism

128
Q

 Hyperthyroidism

A

excess amounts of TH are secreted from the thyroid gland

129
Q
  • Increased metabolic rate
  • Enlargement of the thyroid gland (goiter) caused by stimulation of TSH receptors
  • Primary hyperthyroidism: Grave’s Disease
A

Hyperthyroidism

130
Q
  • Thyroid-stimulating immunoglobulins (TSI) stimulation of TSH receptors in the gland results in hyperplasia of the gland (goiter) and increased synthesis of TH
  • Protrusion of the eyeballs
A

• Primary hyperthyroidism: Grave’s Disease

131
Q

caused by TSH secreting pituitary adenomas

A

• Secondary hyperthyroidism

132
Q

• Symptoms: excitability, weight loss, muscle weakness, protruding eyes

A

 Hyperthyroidism

133
Q

deficient production of TH by the thyroid gland;

A

 Hypothyroidism:

134
Q

: loss of thyroid function (congenital defects)

A

• Primary hypothyroidism

135
Q

: caused by the pituitary’s failure to synthesize adequate amount of TSH (due to pituitary tumors or traumatic brain injury

A

• Secondary hypothyroidism:

136
Q

swelling of the skin and underlying tissues giving a waxy consistency

A

• Myxedema

137
Q

: diminished level of consciousness associated with severe hypothyroidism

A

• Myxedema coma:

138
Q
  • Symptoms: fatigue, increased body weight, slowed HR

* Diagnosis: measure T4 in blood

A

 Hypothyroidism:

139
Q

extreme hypothyroidism in fetal life, infancy or childhood; see inhibited skeletal growth and mental retardation

A

• Cretinism:

140
Q

: secretion is promoted when blood levels glucose increase

A

 Insulin

141
Q

: produced by alpha cells; increases blood glucose concentration; inversely related to insulin

A

 Pancreas: Glucagon

142
Q

characterized by hyperglycemia resulting from defects in insulin secretion/ insulin action

A

 Diabetes Mellitus

143
Q

insulin-dependent; no pancreatic function; beta-cell destruction

A

• Type I DM:

144
Q
  • Most common pediatric chronic disease
  • Increased metabolism of fats and proteins leads to high levels of circulating ketones, causing a condition known as diabetic ketoacidosis (DKA)
  • Weight: nonobese
  • 3 P’s symptoms: polyuria (pee a lot); polyphagia (eat a lot); polydipsia (excessive thirst)
A

• Type I DM:

145
Q

: noninsulin-dependent; partially functioning pancreas; increase risk after age 40

A

• Type II DM

146
Q
  • Risk factors: age, obesity, hypertension, physical inactivity, family history
  • Metabolic syndrome
  • Insulin resistance and decreased insulin secretion by beta cells
  • Increased glucagon secretion
  • KETONES RARE
A

• Type II DM

147
Q

 Can lead to a diabetic coma

A

• Hyperglycemia:

148
Q

 Elevated glucose levels raise plasma osmolality which can manifest as: blurred vision, weight loss, vaginal yeast infections
 If untreated, toxic acids (ketones) can build up in your blood and urine (DKA)
 Clinical goals: prevent glycosuria from occurring

A
  • Acute complications of diabetes:

* Hyperglycemia: elevated glucose levels

149
Q

); deficiency of insulin and an increase in the levels of counterregulatory hormones (glucagon)

A

• Diabetic Ketoacidosis (DKA);

150
Q

 Presence of urine and serum ketones (accumulation of ketones causes a drop in pH, resulting in metabolic acidosis)

A

• Diabetic Ketoacidosis (DKA);

151
Q

 Absence of insulin: fatty acids are converted to ketone bodies; helps out glucagon
 Common in Type I DM

A

• Diabetic Ketoacidosis (DKA);

152
Q

): virtual absence of ketone bodies
 Higher glucose levels then DKA
 More common in Type II DM

A

• Hyperosmolar Coma (HHC):

153
Q

 Because of the amount of insulin required to inhibit fat breakdown is less than that needed for effective glucose transport, insulin levels are sufficient to prevent excessive lipolysis and ketosis

A

• Hyperosmolar Coma (HHC

154
Q

 Usually seek medical treatment a much later date

 Excess urination and extreme elevations of blood sugar levels lead to dehydration throughout the body

A

• Hyperosmolar Coma (HHC

155
Q

 Severe loss of body water can lead to shock, coma, and death

A

 • Hyperosmolar Coma (HHC

156
Q

: insulin shock or insulin reaction
 Causes: extreme exercise or fasting or with large doses of insulin
 Acute response: mediated by counter-regulatory effects of glucagon and catecholamines
 Symptoms: pallor, tremor, anxiety, irritability, fatigue

A

• Hypoglycemia

157
Q

• Microvascular: disease in capillaries
 Nephropathies (end-stage kidney disease)
 Retinopathies (eye becomes progressively opaque, resulting in blurred vision

A

• Chronic Complications of Diabetes:

158
Q

lesions in large- and medium-sized arteries

A

• Macrovascular: • Chronic Complications of Diabetes:

159
Q

 CAD, PVD

 CVA/TIA

A

• Macrovascular: lesions in large- and medium-sized arteries• Chronic Complications of Diabetes:

160
Q

• Neuropathic Disorders: sensory deficits
 Most often damages nerves in your legs and feet
 Pain and numbness in your extremities
 Peripheral/ autonomic neuropathies
 Foot ulcers
 Infections: bacteria LOVE glucose

A

• Chronic Complications of Diabetes: