3rd exam Flashcards

(160 cards)

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
and plasma creatinine concentration are inversely related
 GFR
26
dilation of the renal pelvis and calyces proximal to a blockage leads to ________; enlargement of the renal pelvis and calyces
 Hydronephrosis:
27
cause unobstructed kidney to increase the size of individual glomeruli and tubules but not the total number of functioning nephrons
 Compensatory hypertrophy and hyperfunction
28
(stones): common urinary cause of urinary tract obstruction
 Calculi
29
stones: most common
 Calcium
30
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
 Renal colic
31
 Lower Urinary Tract Obstruction (2)
 Lower Urinary Tract Obstruction  Detrusor hyperreflexia  Stress incontinence
32
neurologic disorders that develop above the pontine
 Detrusor hyperreflexia
33
 Stress incontinence: involuntary loss of urine during coughing, sneezing, laughing, or other physical activity associated with increased abdominal pressure
 Stress incontinence
34
 Complicated UTI (4)
```  Complicated UTI  Escherichia coli  Cloudy urine  Pyelonephritis • Risk factors: urinary obstruction and reflux of urine from the bladder (vesicoureteral reflux) ```
35
: 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
 Complicated UTI
36
most common infecting microorganism
 Escherichia coli | uti
37
: an infection of one or both upper urinary tracts (ureter, pelvis, and interstitium
 Pyelonephritis
38
• Risk factors: UTI
: urinary obstruction and reflux of urine from the bladder (vesicoureteral reflux
39
: inflammation of the glomerulus
 Glomerulonephritis:
40
• Most common type: (acute postinfectious glomerulonephritis)
Streptococcus
41
-antibody complexes; caused by deposition either of circulating antibodies or of antibodies formed in situ to antigens
• Membranous glomerulonephritis
42
anti-glomerular basement membrane disease; associated with antibody formation against both pulmonary capillary and glomerular basement membrane
• Goodpasture syndrome:
43
excretion of 3.5 g or more of protein in the urine per day and is characteristic of glomerular injury
 Nephrotic syndrome:
44
• Disturbances in the glomerular basement membrane and podocyte injury lead to increased permeability to protein and loss of electrical negative charge
Nephrotic syndrome:
45
• Hypoalbuminemia;
proteinuria; edema; hyperlipidemia results | Nephrotic syndrome:
46
: 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
 Acute Kidney Injury
47
associated with hypertension, diabetes mellitus, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies
 Chronic Kidney Injury:
48
systemic symptoms associated with the accumulation of nitrogenous wastes and accumulation of toxins in the plasma caused by the decline in renal function
 Uremia
49
(increased risk of fractures)
 Hypocalcemia
50
decreases red blood cell production and uremia decreases red blood cell life span
 Inadequate production of erythropoietin
51
scratching due to uremic skin residues
 Pruritus
52
a buildup of metabolic waste products occurs when
 When the kidneys do not function efficiently
53
must be excreted daily to prevent toxicity or “hyper” states include, potassium, hydrogen ions and acids
 Electrolytes that must be excreted
54
): the main regulator of the circulating platelet mass; induces platelet production in the bone marrow; platelets express receptors for TPO
 Thrombopoietin (TPO):
55
site of fetal hematopoiesis (blood cell production)
 Spleen:
56
colony-stimulating factors (hematopoietic growth factors); stimulate the proliferation of progenitor cells
 Several cytokines participate in hematopoiesis
57
produced by the kidneys; hormone that stimulates erythrocyte production  In conditions of tissue hypoxia, erythropoietin is secreted by the kidney
 Erythropoietin
58
Fe3+ hemoglobin that cannot bind to oxygen
 Methemoglobin:
59
% of total body iron is bound to heme in erythrocytes (hemoglobin)
 67% of
60
transports iron within the blood; glycoprotein synthesized primarily by the liver but also by tissue macrophages
 Transferrin:
61
: Breakdown of blood clots
 Fibrinolysis
62
digests the fibrin into smaller soluble pieces (fibrin degradation products)
 Plasmin
63
an enzyme that dissolves clots (fibrinolysis) by degrading fibrin and fibrinogen into FDPs
 Plasmin
64
leukocytosis (high levels of circulating leukocytes) often occurs after
 Splenectomy:
65
: most abundant cell in the blood
 Erythrocytes
66
most abundant leukocyte; chief phagocyte in early inflammation
 Neutrophils:
67
: neutrophil, eosinophils, basophils
 Granulocytes:
68
have cytoplasmic granules that contain vasoactive amines (histamine) and anticoagulant (heparin)
 Basophils
69
attacks parasites and fungi
attacks parasites and fungi Eosinophil
70
increased eosinophils due to infections
• Eosinophilia
71
• Most common mechanism is via the parasitic route
• Eosinophilia
72
monocytes, macrophages, lymphocytes, NK cells
 Agranulocytes:
73
: contain cytoplasmic granules capable of releasing proinflammatory biochemical mediators when stimulated by injury to a blood vessel
 Platelets:
74
is necessary for many of the intracellular signaling mechanisms that control platelet activation
 Calcium
75
they are unable to aggregate- a platelet plug cannot be formed with insufficient aggregation
 When platelets degranulate
76
blood flow slows down thus leading to decreased oxygen supply to organs (ischemia)
 Polycythemia Vera: excessive RBCs
77
 Polycythemia Vera treatment
blood transfusions (phlebotomy)
78
 Symptoms: Cerebral thrombosis, viscous blood, chest pain; painful itching
 Polycythemia Vera:
79
 Prognosis: Acute myeloid leukemia (AML), occurring spontaneously in 10% of individuals and generally being resistant to conventional therapy
 Polycythemia Vera:
80
 Primary cause: Epstein-Barr virus  Recovery time: 3 weeks  Symptoms: fatigue, sore throat, fever, lymph node swelling, spleen enlargement
 Mononucleosis: kissing disease
81
malignant disorder of the blood and blood forming organs; WBC cancer  Most common is children
 Leukemia
82
: 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)
 Multiple Myeloma
83
: occurs as myeloma cells replace oxygen carrying RBCs in your bone marrow
 Anemia:  Multiple Myeloma
84
: hypercalcemia; renal injury (M protein); anemia; Bone lesions (lytic- break down of bone)
 Multiple Myeloma |  End organ damage:
85
 General cause of cancer:
SMOKING
86
characterized by enlarged lymphnodes; proliferation of lymphocytes and monocytes
 Lymphadenopathy
87
progression from one group of lymph nodes to another |  Presence of Reed-Sternberg (RS) cells
 Hodgkin Lymphoma
88
 Symptoms: intermittent fever, drenching night sweats, itchy skin (pruritus), and fatigue
 Hodgkin Lymphoma
89
(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
 Disseminated intravascular coagulation
90
 Results from a “consumption of clotting factors”
 Disseminated intravascular coagulation (DIC):
91
 Insufficient factors available to complete the extrinsic and intrinsic coagulation cascades resulting in “microvascular bleeding” that can be life threatening
Disseminated intravascular coagulation (DIC):
92
 Causes: Human Papillomavirus (HPV) infection
 Cervical cancer:
93
 Stages of cancer (overall):
 (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
 Mainly stored in liver (20 years worth of B12)  Nasty coded tongue; nerve damage if not correct  Dark green leafy vegetables contain B12
 B12 Deficiency: problem is pregnancy
95
 Certain cancers are more likely to occur when
when a chronic disease is present
96
increase the risk of developing colon cancer
 Chrohn’s disease and ulcerative colitis increase
97
 In males, without GnRH, ---- cannot be secreted
FSH
98
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.
 Thyroid-stimulating hormone (TSH)
99
 Water soluble homones:
protein homrones
100
 Circulate throughout the body in unbound form
 Water soluble homones: protein homrones
101
 Act as first messengers, binding to receptors on the cell’s plasma membrane
 Water soluble homones: protein homrones
102
 The signals initiated by hormone-receptor binding are then transmitted into the cell by the action of second messengers
 Water soluble homones: protein homrones
103
Thyroid hormones and steroids (cortisol):
 Lipid-soluble hormones
104
 Circulate throughout the body bound to carrier proteins
 Lipid-soluble hormones
105
 Cross the plasma membrane by diffusion
 Lipid-soluble hormones
106
 Diffuse directly into the cell nucleus and bind to nuclear receptors
 Lipid-soluble hormones
107
low concentrations of hormone increase the number of receptors per cell
 Up-regulation
108
: high concentrations of a hormone decrease the number of receptors
 Down-regulation
109
 Anterior pituitary: produces (6)
GH, ACTH, TSH, FSH, LH, prolactin
110
 Posterior pituitary: produces (2)
ADH, oxytocin
111
ACTH regulates (check)
the release of cortisol from the adrenal cortex
112
regulates the activity of the thyroid glad
• TSH:
113
causes uterine contraction and lactation in women and may have a role in sperm motility
• Oxytocin
114
• 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
Oxytocin
115
: increased water reabsorption
• ADH
116
• 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
ADH
117
: insufficient activity of ADH leading to polyuria
 Diabetes insipidus:
118
* 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
Diabetes insipidus:
119
lowers serum calcium levels by inhibition of bone-resorbing osteoclasts
 Thyroid: Calcitonin
120
• Secretion is regulated by TRH through negative feedback loop that involves the anterior pituitary and hypothalamus
 TH:
121
: necessary for TH synthesis
• Iodine:
122
): glycoprotein that is the precursor of TH; combines with iodine
• Thyroglobulin (TG):
123
transports TH within the blood
• Thyroxine-binding globulin (TBG
124
• Secretion of T3 and T4 controlled by
TSH
125
• Physiologic Function: metabolic rates of all cells; causes synthesis of enzymes, proteins and other substances
 TH:
126
• Secretion is regulated by TRH through negative feedback loop that involves the anterior pituitary and hypothalamus
 TH:
127
can cause mental retardation and stunts physical growth
 Congenital Hypo and Hyperthyroidism
128
 Hyperthyroidism
excess amounts of TH are secreted from the thyroid gland
129
* Increased metabolic rate * Enlargement of the thyroid gland (goiter) caused by stimulation of TSH receptors * Primary hyperthyroidism: Grave’s Disease
Hyperthyroidism
130
* 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
• Primary hyperthyroidism: Grave’s Disease
131
caused by TSH secreting pituitary adenomas
• Secondary hyperthyroidism
132
• Symptoms: excitability, weight loss, muscle weakness, protruding eyes
 Hyperthyroidism
133
deficient production of TH by the thyroid gland;
 Hypothyroidism:
134
: loss of thyroid function (congenital defects)
• Primary hypothyroidism
135
: caused by the pituitary’s failure to synthesize adequate amount of TSH (due to pituitary tumors or traumatic brain injury
• Secondary hypothyroidism:
136
swelling of the skin and underlying tissues giving a waxy consistency
• Myxedema
137
: diminished level of consciousness associated with severe hypothyroidism
• Myxedema coma:
138
* Symptoms: fatigue, increased body weight, slowed HR | * Diagnosis: measure T4 in blood
 Hypothyroidism:
139
extreme hypothyroidism in fetal life, infancy or childhood; see inhibited skeletal growth and mental retardation
• Cretinism:
140
: secretion is promoted when blood levels glucose increase
 Insulin
141
: produced by alpha cells; increases blood glucose concentration; inversely related to insulin
 Pancreas: Glucagon
142
characterized by hyperglycemia resulting from defects in insulin secretion/ insulin action
 Diabetes Mellitus
143
insulin-dependent; no pancreatic function; beta-cell destruction
• Type I DM:
144
* 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)
• Type I DM:
145
: noninsulin-dependent; partially functioning pancreas; increase risk after age 40
• Type II DM
146
* 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
• Type II DM
147
 Can lead to a diabetic coma
• Hyperglycemia:
148
 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
* Acute complications of diabetes: | * Hyperglycemia: elevated glucose levels
149
); deficiency of insulin and an increase in the levels of counterregulatory hormones (glucagon)
• Diabetic Ketoacidosis (DKA);
150
 Presence of urine and serum ketones (accumulation of ketones causes a drop in pH, resulting in metabolic acidosis)
• Diabetic Ketoacidosis (DKA);
151
 Absence of insulin: fatty acids are converted to ketone bodies; helps out glucagon  Common in Type I DM
• Diabetic Ketoacidosis (DKA);
152
): virtual absence of ketone bodies  Higher glucose levels then DKA  More common in Type II DM
• Hyperosmolar Coma (HHC):
153
 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
• Hyperosmolar Coma (HHC
154
 Usually seek medical treatment a much later date |  Excess urination and extreme elevations of blood sugar levels lead to dehydration throughout the body
• Hyperosmolar Coma (HHC
155
 Severe loss of body water can lead to shock, coma, and death
 • Hyperosmolar Coma (HHC
156
: 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
• Hypoglycemia
157
• Microvascular: disease in capillaries  Nephropathies (end-stage kidney disease)  Retinopathies (eye becomes progressively opaque, resulting in blurred vision
• Chronic Complications of Diabetes:
158
lesions in large- and medium-sized arteries
• Macrovascular: • Chronic Complications of Diabetes:
159
 CAD, PVD |  CVA/TIA
• Macrovascular: lesions in large- and medium-sized arteries• Chronic Complications of Diabetes:
160
• 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
• Chronic Complications of Diabetes: