Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SRNA3AdvancedPatho2 > EXAM 2 THYROID DISORDERS > Flashcards

EXAM 2 THYROID DISORDERS Flashcards

1
Q

What are the 4 types of Hyperthyroidism (thyrotoxicosis) ?

A
  • Primary
  • Secondary
  • Subclinical
  • Thyroid Storm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the characteristics of Primary Hyperthyrodisim as far as TSH and T3 and T4? other names

A

Primary ↑T3 ↑T4 ↓TSH (Grave’s, Multi-Nodular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the characteristics of Secondary Hyperthyrodisim as far as TSH and T3 and T4? other names

A

Secondary ↑T3T4 ↑ TSH (“Central”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the characteristics of SUBCLINICAL Hyperthyrodisim?

A

Subclinical (Asymptomatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the characteristics of Thyroid Storm?

A

Thyrotoxic crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the types of Hypothyroidism?

A

– Primary
– Secondary
– Congenital
– Iatrogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the cause of primary hypothyroidism?

A

↓ iodine, Hashimoto’s, carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 types of Hyperparathyroidism?

A

– Primary – Secondary – Tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thyroid connected by ______At _______

A

•Connected by isthmus at cricoid cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can you distinguish C cells?

A

Can be distinguished from surrounding follicular cells by its place cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Found around the follicles?

A

Blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Follicular epithelium is

A

simple, low cuboidal or squamous . During active secretory phases , become columnar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypothyroidism and ventilation

A

In Hypothyroidism, ventilation can become severely depressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does Calcitonin decreases Calcium level?

A

By inhibiting osteoclas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is PTH secreted?

A

Stimulated by decrease in calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

During low calcium, in bone what happens?

A

PTH first stimulates osteoblasts

RESULTS IN OSTEOCLAST ACTIVATION RELEASING CA2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

During low calcium, in Kidneys what happens?

A

Increase reabsorption of Ca2+
Decrease reabsoprtion of phosphorus and bicarbonate
Increase D3 conversion to active Vit D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

During low calcium, in GIT what happens?

A

Increase absorption of Ca2+ from intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What cells produce Thyroglobulin?

A

Follicular cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Can exacerbate symptoms in thyroid disease?

A

Repetitive palpation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Grave’s disease associated with?

A

Increase T3, T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes Grave’s disease?

A

Caused by antibodies

  • **TSI (Thyroid stimulating immunoglobulin)
  • **Stimulate TSH receptors on thyroid gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical manifestations of Grave’s disesae

A

Goiter- Enlarged thyroid glan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TSI overstimulation of TSH receptors results in

A

Hypertrophy and Hyperplasi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

**Airway issues with Goiter?

A

Distortion of the laryngeal inlet
Deviation of the trachea
Erosion of tracheal rings (trachelomalacia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

TO assess Goiter

A

CXR

Xray/CT scan of neck: allow good Assessment of airway distortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

As thyroid enlarges, what occurs with trachea?

A

Displaces trachea posteriorly and pushes larynx cephalad, making laryngeal inlet easir to view

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Opthalmopathy is a manifestation of

A

Grave’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

2 types of Opthalmopathy

A

Functional

Infiltrative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Functional Opthalmopathy

A

Hyperactive sympathetic branch
Lag of globe on upward gaze
Lag of upper lid on downward gaze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Infiltrative Opthalmopathy

A

TSI react with orbital Fibroblasts = EXOPHTALMOS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Infiltrative opthalmopathy include exophtalmos as evidenced by

A

Protrusion of the eyeballs from
•Enlarged ocular muscles
•Increased orbital fat
•Inflammation/Edema of orbital contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Graves Exophtalmos may be associated with

PPPP CBD, LVED

A 
Periorbital Edema
Pain irritation
Photophobia
Papilledema
Corneal Ulceration 
Blurred vison
Diplopia
Lacrimation
Visual field impairment 
Exposure Keratosis
Decreased visual acuity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Clinical manifestations of Grave’s disease: Pretibial myxedema

A

– Sub-Q erythema & swelling over anterior legs
– TSI activate thyrotropin receptor antigens on
fibroblasts (causes ↑ hyaluronic acid production)
– TSI recruitment of T lymphocytes (causes induration)
(Glucocorticoids helpful for skin and eye changes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Clinical manifestations of Grave’s disease:Acropachy

A

– Same process may occur in hands causing clubbing of fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Graves Treatment Beta Blockers

A

Beta blockers
– Propranolol (sympathetic tachycardia/nausea)
(also inhibits T4 conversion to T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Grave’s Treatment Radioactive iodine

A

– Iodine131 (destroys thyroid over weeks to months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Grave’s Treatment: Antithyroid drugs

A

– Methimazole, propylthiouracil (blocks iodination or conversion of T4 to T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Grave’s Treatment surgical

A

Surgical Thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is multinodular

A

Thyroid follicls increase in response to increase TSH and normally return to original size when TSH levels normalize again–> Results in hyperfunctioning follicular nodules producing excess T3, T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

In Multinodular, If only one nodule hyperfunctioning =

A

Solitary Toxic adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Multinodular and malignancy

A

High incidence of malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Biopsy recommended for multinodular

A

Fine needle aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Treatments of multinodular

A

Radioactive Iodine, Antithyroid drugs, Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Secondary Hyperthyroidism

a.ka.

A

Central
pituitary adenoma over producing TSH
Increase TSH = increase T3T4
TRH decreases through Negative feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Secondary hyperthyroidism Other causes: Gestational thyrotoxicosis

A

Gestational thyrotoxicosis – ↑HCG can stimulate TSH receptor on thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Subclinical Hyperthyroidism is

A

Normal to slightly elevated T3,t4, decreased TSH

Negative feedback results in decrease TS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Thyroid Storm is a

A

Thyrotoxic crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Thyrotoxic crisis death can occur

A

within 48 hours without treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

When does thyrotoxic crisis occur?

A

Usually occurs in undiagnosed or partially treated pts. with severe Hyperthyroidism who are subjected to excessive stress from other causes: surgery, infections, pulmonary or
cardiovascular disorders, trauma, burns, seizures, obstetric complications, emotional distress or dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

HyperThyroids Signs and Symptoms

A
  • Hyperthermia
  • Hypertension
  • Tachycardia
  • Arrhythmia
  • Agitation
  • Delirium
  • N/V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

When in doubt

A

Dandrolene should be considered without delay to Recognize and treat MH early can result in death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Dantrolene effectively

A

reduces temperature but doesn’t ameliorate cardiovascular disturbances. Also has adverse effects of muscle weakness and N/V.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What does NOT occur with multinodular

A

Exopthalmos and Pretibial Myexdema do not occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)

Rise in temperature

A

Early, severe
Late severe
Early, mild , moderate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)

Hypertension

A

Moderate, wide pulse pressure
Moderate, narrow pulse pressure
Severe, mainly systolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)

Tachycardia

A

Severe
Moderate
Severe tachycardia or bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)

Arrythmia

A

Mainly atrial, possible atrial fibrillation
Mainly ventricular
Atrial and ventricular can occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)

PaCO2

A

Moderate elevation
Severe elevation
Mild elevation

60
Q

Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)

pH

A

Normal
Acidosis
Normal

61
Q

Histologically similar to pretibial myxedema

A

Hypothyroidism

62
Q

Hypothyroidism symptoms

A

Also causes thickening of tongue, laryngeal and

pharyngeal mucus membranes.

63
Q

Hypothyroidism – Possible ECG changes

A
  • Decreased P waves & QRS complex
  • Flat or inverted T waves
  • Prolonged QT interval
  • Torsade de pointes
  • Bradycardia
64
Q

Hypothyroidism – Possible ECG changes why?

A

Recall effects of T3 on myocardium

65
Q

Iodine Deficiency is caused by

A

• Caused by ↓ Iodine intake

66
Q

What is the most common cause of worldwide

A

Iodine deficiency

67
Q

Iodine Minimum daily intake

A

150mcg

68
Q

Iodine sources:

A 
Seaweed
Iodized salt
Cod fish,
Cranberries 
Yogurt, 
potatoes
turkey
navy beans
69
Q

What happens to Hashimoto’s Disease?a.

A

Autoantibodies form against thyroid peroxidase and thyroglobulin.

70
Q

What does Hashimoto’s Disease cause?

A

Causes inflammation and destruction of follicular

cells.

71
Q

Hashimoto’s Disease

A

Individuals genetically predisposed.

72
Q

Hashimoto’s Disease Associated with

A 
High iodine intake
Selenium deficiency
Smoking 
Chronic hepatitis C
Interferon-alpha
73
Q

In Hashimoto’s Damaged cells
• First causing transient thyrotoxicosis followed by
hypothyroidism.
• Treatment: replacement thyroid hormone

A

leak T3T4 into bloodstream.

74
Q

Other drugs associated with Hashimoto’s:

A

lithium, amiodarone, cholestyramine

75
Q

The damaged cells lead to leaking of T3 and T4 in the bloodstream, First causing

A

Transient thyrotoxicosis followed by hypothyroidism.

76
Q

Most common endocrine malignancy.

A

Thyroid Carcinoma

77
Q

What can cause thyroid carcinoma? What does most patients have?

A

Exposure to ionizing radiation, especially during childhood.

Most pts. Have normal levels T3 T4

78
Q

Thyroid Carcinoma usually discovered as

A

small nodule or metastatic tumor in regional lymph nodes, lungs, brain or bone.

79
Q

What are the Signs/Symptoms of Thyroid Carcinoma

A
  • Changes in voice and swallowing
  • Difficulty breathing
  • Diagnosis is by fine needle aspiration
80
Q

Treatment of thyroid Carcinoma

A

Partial or total thyroidectomy;
Post-op radioactive iodine to treat any residual tumor cells.
TH replacement with Levothyroxine

81
Q

Secondary Hypothyroidism is a

A

• Failure of hypothalamus and/or pituitary

82
Q

In secondary hypothyroidism , TRH, TSH, T3,T4

A

↓TRH and/or
↓TSH results in
↓T3T

83
Q

Often misdiagnosed and treated as primary, resulting in destruction of thyroid gland.

A

Secondary Hypothyroidism

84
Q
  • Occurs less commonly.

* Treatment depends on cause.

A

Secondary Hypothyroidism

85
Q

Congenital Hypothyroidism is a.
• Symptoms may not be evident until 4 months
of age.

A

• Thyroid hormone deficiency at birth

86
Q

Congenital Hypothyroidism is caused by

A

thyroid agenesis or hereditary defect in TH synthesis.

87
Q

Congenital Hypothyrodism results in

A

• Results in Cretinism.

88
Q

TH necessary for development of________What happens to infant?

A

Brain tissue. Infant will be mentally retarded if no T4

available during fetal life

89
Q

Congenital Hypothyroidism

• Signs/Symptoms:

A

– Hypothermia
– Delay in passing meconium
– Neonatal jaundice

90
Q

Congenital Hypothyroidism Without treatment:

A
  • Decreased eating
  • Hoarse cry
  • Myxedema of oral tissues and vocal cords
91
Q

Congenital - Cretinism (DAPUH)

• In the adult:

A
  • Dwarfism
  • Abdominal protrusion
  • Poor overall development
  • Umbillical herniation
  • Hypothyroidism
92
Q

Iatrogenic Hypothyroidism (TARS)

A
  • ↓TH secondary to treatment
  • Antithyroid Drugs
  • Radioactive Iodine therapy
  • Sequella of Surgery
93
Q

Hyperparathyroidism

– General Effects of Hypercalcemia

A 
Affects Muscle, Bone, Nerve, GI systems:
• Fatigue
• HA
• Depression
• Anorexia
• N/V
• Cardiovascular ds.
• HTN
• Pathologic fractures
94
Q

Anesthesia Note with the general effects of hypercalcemia

A

Anesthesia Note: Hypercalcemia may antagonize non-depolarizing muscle relaxants. Continuous monitoring of neuromuscular blockade recommended.

95
Q

Primary Hyperparathyroidism :

A

Primary ↑Ca, ↓Phos

96
Q

Primary Hyperparathyroidism hormones and electrolytes imbalance

A

↑PTH = Hypercalcemia, Hypophosphatemia

97
Q

Primary Hyperparathyroidism is a________ disease
and there is
and

A

Sporadic
Excess production PTH by one or more PT glands
Loss of feedback control

98
Q

Primary Hyperparathyroidism % adenoma and hyperplasia

A

• 85% PT adenoma, 15% PT hyperplasia

99
Q

In Primary Hyperparathyroidism what happens to phos –>

A

• ↓Phos due to ↑ ↑ ↑ urinary excretion of Phosphate• Increased Phosphate depletion impairs tubular
reabsorption of Bicarbonate = Metabolic Acidosis

100
Q

Secondary Hyperparathyroidism : electrolyte Ca and phos

A

Secondary ↓Ca, ↑Phos

101
Q

Secondary Hyperparathyroidism is

A

↑PTH secondary to other Ca lowering diseases
(ex. chronic kidney ds., intestinal malabsorption)
• Hypocalcemia due to secondary disease.
• Hyperphosphatemia due to glomerular filtration
failure.

102
Q

• Other causes of Secondary Hyperparathyroidism

A

Phenytoin, phenobarbital,
laxatives – accelerate Vit. D catabolism or
decrease intestinal absorption of Ca.

103
Q

Tertiary Hyperparathyroidism electrolyte imbalance

•

A

↑Ca

104
Q

Tertiary Hyperparathyroidism

A
  • Occurs following long-standing Secondary HPT

* Subsequently results later in Hypercalcemia

105
Q

Etiology of Tertiary Hyperparathyroidism ? What does it present with? Normally PT tissues is not

A

is unknown. Presents with unusual persistent autonomous secretion of PTH. Normally PT tissue is not autonomous and only responds to physiologic stimulus of
hypocalcemia.

106
Q

HYPOPARATHYROIDISM: Phos and Ca

A

↓Ca, ↑Phos

107
Q

Hypoparathyroidism there is ______ caused by

A

↓PTH
• Caused by damage to PT gland during thyroid
surgery

108
Q

Explain the electrolyte imbalance with hypoparathyroidism

A

• Hypocalcemia
• Hyperphosphatemia due to loss of PTH effects
at kidney. (Normally PTH↑ urinary excretion of Phosphate).

109
Q

Hypoparathyrodism: Hyper and hypopara

A

↓Ca, ↑Phos like secondary hyperpara, but

without renal failure = hypopara

110
Q

Hypocalcemia lowers

A

• Lowers threshold for nerve and muscle
excitation. Even slight stimulus can initiate
nerve impulse.

111
Q

Hypocalcemia Creates Tetany:

A 
– Muscle spasms 
– Hyperreflexia 
– Tonic-clonic convulsions 
– Laryngeal spasms 
– Death from asphyxiation
112
Q

Hypocalcemia signs

A

• Chvostek and Trousseau signs evaluate

neuromuscular irritability

113
Q

Treat hypocalcemia Treat with

A

• Treatment: calcium and Vit. D

114
Q

Most popular technique for thyroid surgery is

A

General anesthesia.

115
Q

Regional anesthesia possible with cervical plexus block, but carries risks (4)

A

– Vocal cord dysfunction from block
– Damage to vertebral artery
– Damge to phrenic nerve
– Damage to S.C.

116
Q

Anesthesia Considerations - Airway

Goiters may cause (4)

A

– Tracheal deviation
– Distortion of laryngeal inlet
– Erosion Erosion of tracheal rings of tracheal rings
– post -op airway collapse

117
Q

What do you do on Extubation for Thyroid?

A

On Extubation:
– Check vocal cord function before removing pt.
from O.R.
– Direct laryngoscopy generally requires bolus of
propofol.
– Alternatively, LMA can be used with endoscope

118
Q

Thyroid disorder: Anesthesia Considerations - Positioning.

Airway

A

Once airway secured, pt. usually positioned with
padding under shoulders; and neck extended on
a head ring

119
Q

Thyroid disorder: Anesthesia Considerations - Positioning.

• Sterile draping generally includes

A

split towel wrapped around the head, this will require

disconnect from anesthesia circuit and subsequent positioning of the pt.

120
Q

Thyroid disorder: Anesthesia Considerations - Positioning: Movement

A

Movement can cause endotracheal tube to become displaced. Its proper positioning must be rechecked before surgery commences.

121
Q

Regional anesthesia possible with cervical plexus block, but carries risks (4)

A

– Vocal cord dysfunction from block
– Damage to vertebral artery
– Damge to phrenic nerve
– Damage to S.C.

122
Q

Anesthesia Considerations - Airway

Goiters may cause (4)

A

– Tracheal deviation
– Distortion of laryngeal inlet
– Erosion Erosion of tracheal rings of tracheal rings
– post -op airway collapse

123
Q

What do you do on Extubation for Thyroid?

A

On Extubation:
– Check vocal cord function before removing pt.
from O.R.
– Direct laryngoscopy generally requires bolus of
propofol.
– Alternatively, LMA can be used with endoscope

124
Q

Thyroid disorder: Anesthesia Considerations - Positioning.

Airway

A

• Once airway secured, pt. usually positioned with
padding under shoulders; and neck extended on
a head ring

125
Q

Thyroid disorder: Anesthesia Considerations - Positioning.

• Sterile draping generally includes

A

split towel wrapped around the head, this will require

disconnect from anesthesia circuit and subsequent positioning of the pt.

126
Q

Thyroid disorder: Anesthesia Considerations - Positioning: Movement

A

Movement can cause endotracheal tube to become displaced. Its proper positioning must be rechecked before surgery commences.

127
Q

Why does hyperthyroidism medications takes a long time to take effect?

A

Destroys glands over time not overnight

Slow death of gland

128
Q

Pt has breast cancer, uncontrolled amounts of parathyroid hormone related peptide. Why are they drawing blood for calcium

A

Tooo high because cancer cells are causing increase production.

129
Q

HOw can little gland in neck makes my bones weak.

A

CAlcium regulation, increase blood calcium, decrease bone CA make then weak and they break

130
Q

Blowing BP cuff and looking at hand

A

Checking trousseau sign to screen for low CA, (carpopedal spasm)

131
Q

Why labs check for level of proteins?

A

Thyroid + steroid need transport proteins hormones

132
Q

Most likely to happen with body weight and tolerance of heat and cold when the gland is destroyed

A

Hypothyroidism

Weight gain and cold intolerance.

133
Q

Hypothyroidism on P wave and QRS

A 
Decrease p wave
Decrease QRS complex
Increase QT
Torsade 
Bradycardia
134
Q

Hyperthyroidism on CV

A

Tachy
Increase rate and output
Cardiomyopathy

135
Q

Why does people with hyperparathyroidism are predisposed to form kidney stones

A

Increase blood Ca levels

Increase resorption of Ca in DCT

136
Q

What is the difference between Thyrotoxicosis and Thyrotoxic crisis?

A

Thyrotoxicosis -> Hyperthyroidism

Thyrotoxic crisis–> Thyroid storm (death within 48 hrs, undiagnosed

137
Q

When tumor destroys thyroid gland what happens to thyroid glands, blood lvels of TRH

A

TSH

and TRH goes up

138
Q

↓TH leads to

A

↑TSH – could cause goiter.

139
Q

• Treatment with iodine replacement. If goiter is

present

A

additional treatment

140
Q

Hyperparathyroidism Signs and symptoms

A

Fatigue, HA, Depressio, Anorexia, NV, CV disease, HTN , pathologic fractures

141
Q

Hypoparathyroidism Signs and symptoms

A

Tetany, Chovesk sign (face),. Trousseau, (arm) Tracheal deviation, distortion of laryngeal inlet, erosion of tracheal rings.

142
Q

Enlargement of the thyroid gland is called a _____and is a response to increased stimulation by

A

Goiter ; TSI (overstimulation of TSH)

143
Q

Cretinism is caused by untreated

A

Congenital Hyperthyroidism

144
Q

Calcitonin is secreated by the _________and help regulate plasma ____concentration

A

Thyroid glands ; Calcium

145
Q

Role of beta blockers in the treatment of Hyperthyrodism

A

Propranolol
Inhibits T4 conversion to T3
sympathetic tachycardia and nausea

146
Q

What are the neuromuscular signs and symptoms of hyperparathyroidism

A

Increase Ca may antagonize, NDNMBA continue monitoring

SRNA3AdvancedPatho2 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions