EXAM 2 THYROID DISORDERS Flashcards
1
Q
What are the 4 types of Hyperthyroidism (thyrotoxicosis) ?
A
- Primary
- Secondary
- Subclinical
- Thyroid Storm
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)
3
Q
What are the characteristics of Secondary Hyperthyrodisim as far as TSH and T3 and T4? other names
A
Secondary ↑T3T4 ↑ TSH (“Central”)
4
Q
What are the characteristics of SUBCLINICAL Hyperthyrodisim?
A
Subclinical (Asymptomatic)
5
Q
What are the characteristics of Thyroid Storm?
A
Thyrotoxic crisis
6
Q
What are the types of Hypothyroidism?
A
– Primary
– Secondary
– Congenital
– Iatrogenic
7
Q
What are the cause of primary hypothyroidism?
A
↓ iodine, Hashimoto’s, carcinoma
8
Q
What are the 3 types of Hyperparathyroidism?
A
– Primary – Secondary – Tertiary
9
Q
Thyroid connected by ______At _______
A
•Connected by isthmus at cricoid cartilage
10
Q
How can you distinguish C cells?
A
Can be distinguished from surrounding follicular cells by its place cytoplasm
11
Q
Found around the follicles?
A
Blood vessels
12
Q
Follicular epithelium is
A
simple, low cuboidal or squamous . During active secretory phases , become columnar
13
Q
Hypothyroidism and ventilation
A
In Hypothyroidism, ventilation can become severely depressed
14
Q
How does Calcitonin decreases Calcium level?
A
By inhibiting osteoclas
15
Q
When is PTH secreted?
A
Stimulated by decrease in calcium
16
Q
During low calcium, in bone what happens?
A
PTH first stimulates osteoblasts
RESULTS IN OSTEOCLAST ACTIVATION RELEASING CA2+
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
18
Q
During low calcium, in GIT what happens?
A
Increase absorption of Ca2+ from intestine
19
Q
What cells produce Thyroglobulin?
A
Follicular cell
20
Q
Can exacerbate symptoms in thyroid disease?
A
Repetitive palpation
21
Q
Grave’s disease associated with?
A
Increase T3, T4
22
Q
What causes Grave’s disease?
A
Caused by antibodies
- **TSI (Thyroid stimulating immunoglobulin)
- **Stimulate TSH receptors on thyroid gland
23
Q
Clinical manifestations of Grave’s disesae
A
Goiter- Enlarged thyroid glan
24
Q
TSI overstimulation of TSH receptors results in
A
Hypertrophy and Hyperplasi
25
****Airway issues with Goiter?
Distortion of the laryngeal inlet
Deviation of the trachea
Erosion of tracheal rings (trachelomalacia)
26
TO assess Goiter
CXR
| Xray/CT scan of neck: allow good Assessment of airway distortion
27
As thyroid enlarges, what occurs with trachea?
Displaces trachea posteriorly and pushes larynx cephalad, making laryngeal inlet easir to view
28
Opthalmopathy is a manifestation of
Grave's disease
29
2 types of Opthalmopathy
Functional
| Infiltrative
30
Functional Opthalmopathy
Hyperactive sympathetic branch
Lag of globe on upward gaze
Lag of upper lid on downward gaze
31
Infiltrative Opthalmopathy
TSI react with orbital Fibroblasts = EXOPHTALMOS
32
Infiltrative opthalmopathy include exophtalmos as evidenced by
Protrusion of the eyeballs from
•Enlarged ocular muscles
•Increased orbital fat
•Inflammation/Edema of orbital contents
33
Graves Exophtalmos may be associated with
| PPPP CBD, LVED
```
Periorbital Edema
Pain irritation
Photophobia
Papilledema
Corneal Ulceration
Blurred vison
Diplopia
Lacrimation
Visual field impairment
Exposure Keratosis
Decreased visual acuity
```
34
Clinical manifestations of Grave's disease: Pretibial myxedema
– 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)
35
Clinical manifestations of Grave's disease:Acropachy
– Same process may occur in hands causing clubbing of fingers
36
Graves Treatment Beta Blockers
Beta blockers
– Propranolol (sympathetic tachycardia/nausea)
(also inhibits T4 conversion to T3
37
Grave's Treatment Radioactive iodine
– Iodine131 (destroys thyroid over weeks to months
38
Grave's Treatment: Antithyroid drugs
– Methimazole, propylthiouracil (blocks iodination or conversion of T4 to T3
39
Grave's Treatment surgical
Surgical Thyroidectomy
40
What is multinodular
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
41
In Multinodular, If only one nodule hyperfunctioning =
Solitary Toxic adenoma
42
Multinodular and malignancy
High incidence of malignancy
43
Biopsy recommended for multinodular
Fine needle aspiration
44
Treatments of multinodular
Radioactive Iodine, Antithyroid drugs, Surgery
45
Secondary Hyperthyroidism
| a.ka.
Central
pituitary adenoma over producing TSH
Increase TSH = increase T3T4
TRH decreases through Negative feedback
46
Secondary hyperthyroidism Other causes: Gestational thyrotoxicosis
Gestational thyrotoxicosis – ↑HCG can stimulate TSH receptor on thyroid gland
47
Subclinical Hyperthyroidism is
Normal to slightly elevated T3,t4, decreased TSH
| Negative feedback results in decrease TS
48
Thyroid Storm is a
Thyrotoxic crisis
49
Thyrotoxic crisis death can occur
within 48 hours without treatment
50
When does thyrotoxic crisis occur?
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
51
HyperThyroids Signs and Symptoms
* Hyperthermia
* Hypertension
* Tachycardia
* Arrhythmia
* Agitation
* Delirium
* N/V
52
When in doubt
Dandrolene should be considered without delay to Recognize and treat MH early can result in death.
53
Dantrolene effectively
reduces temperature but doesn’t ameliorate cardiovascular disturbances. Also has adverse effects of muscle weakness and N/V.
54
What does NOT occur with multinodular
Exopthalmos and Pretibial Myexdema do not occur.
55
Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)
| Rise in temperature
Early, severe
Late severe
Early, mild , moderate
56
Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)
| Hypertension
Moderate, wide pulse pressure
Moderate, narrow pulse pressure
Severe, mainly systolic
57
Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)
| Tachycardia
Severe
Moderate
Severe tachycardia or bradycardia
58
Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)
| Arrythmia
Mainly atrial, possible atrial fibrillation
Mainly ventricular
Atrial and ventricular can occur
59
Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)
| PaCO2
Moderate elevation
Severe elevation
Mild elevation
60
Thyrotoxis vs Malignant vs Pheochromocytoma (TMP)
| pH
Normal
Acidosis
Normal
61
Histologically similar to pretibial myxedema
Hypothyroidism
62
Hypothyroidism symptoms
Also causes thickening of tongue, laryngeal and
| pharyngeal mucus membranes.
63
Hypothyroidism – Possible ECG changes
* Decreased P waves & QRS complex
* Flat or inverted T waves
* Prolonged QT interval
* Torsade de pointes
* Bradycardia
64
Hypothyroidism – Possible ECG changes why?
Recall effects of T3 on myocardium
65
Iodine Deficiency is caused by
• Caused by ↓ Iodine intake
66
What is the most common cause of worldwide
Iodine deficiency
67
Iodine Minimum daily intake
150mcg
68
Iodine sources:
```
Seaweed
Iodized salt
Cod fish,
Cranberries
Yogurt,
potatoes
turkey
navy beans
```
69
What happens to Hashimoto’s Disease?a.
Autoantibodies form against thyroid peroxidase and thyroglobulin.
70
What does Hashimoto's Disease cause?
Causes inflammation and destruction of follicular
| cells.
71
Hashimoto's Disease
Individuals genetically predisposed.
72
Hashimoto's Disease Associated with
```
High iodine intake
Selenium deficiency
Smoking
Chronic hepatitis C
Interferon-alpha
```
73
In Hashimoto's Damaged cells
• First causing transient thyrotoxicosis followed by
hypothyroidism.
• Treatment: replacement thyroid hormone
leak T3T4 into bloodstream.
74
Other drugs associated with Hashimoto's:
lithium, amiodarone, cholestyramine
75
The damaged cells lead to leaking of T3 and T4 in the bloodstream, First causing
Transient thyrotoxicosis followed by hypothyroidism.
76
Most common endocrine malignancy.
Thyroid Carcinoma
77
What can cause thyroid carcinoma? What does most patients have?
Exposure to ionizing radiation, especially during childhood.
| Most pts. Have normal levels T3 T4
78
Thyroid Carcinoma usually discovered as
small nodule or metastatic tumor in regional lymph nodes, lungs, brain or bone.
79
What are the Signs/Symptoms of Thyroid Carcinoma
* Changes in voice and swallowing
* Difficulty breathing
* Diagnosis is by fine needle aspiration
80
Treatment of thyroid Carcinoma
Partial or total thyroidectomy;
Post-op radioactive iodine to treat any residual tumor cells.
TH replacement with Levothyroxine
81
Secondary Hypothyroidism is a
• Failure of hypothalamus and/or pituitary
82
In secondary hypothyroidism , TRH, TSH, T3,T4
↓TRH and/or
↓TSH results in
↓T3T
83
Often misdiagnosed and treated as primary, resulting in destruction of thyroid gland.
Secondary Hypothyroidism
84
* Occurs less commonly.
| * Treatment depends on cause.
Secondary Hypothyroidism
85
Congenital Hypothyroidism is a.
• Symptoms may not be evident until 4 months
of age.
• Thyroid hormone deficiency at birth
86
Congenital Hypothyroidism is caused by
thyroid agenesis or hereditary defect in TH synthesis.
87
Congenital Hypothyrodism results in
• Results in Cretinism.
88
TH necessary for development of________What happens to infant?
Brain tissue. Infant will be mentally retarded if no T4
| available during fetal life
89
Congenital Hypothyroidism
| • Signs/Symptoms:
– Hypothermia
– Delay in passing meconium
– Neonatal jaundice
90
Congenital Hypothyroidism Without treatment:
* Decreased eating
* Hoarse cry
* Myxedema of oral tissues and vocal cords
91
Congenital - Cretinism (DAPUH)
| • In the adult:
* Dwarfism
* Abdominal protrusion
* Poor overall development
* Umbillical herniation
* Hypothyroidism
92
Iatrogenic Hypothyroidism (TARS)
* ↓TH secondary to treatment
* Antithyroid Drugs
* Radioactive Iodine therapy
* Sequella of Surgery
93
Hyperparathyroidism
| – General Effects of Hypercalcemia
```
Affects Muscle, Bone, Nerve, GI systems:
• Fatigue
• HA
• Depression
• Anorexia
• N/V
• Cardiovascular ds.
• HTN
• Pathologic fractures
```
94
Anesthesia Note with the general effects of hypercalcemia
Anesthesia Note: Hypercalcemia may antagonize non-depolarizing muscle relaxants. Continuous monitoring of neuromuscular blockade recommended.
95
Primary Hyperparathyroidism :
Primary ↑Ca, ↓Phos
96
Primary Hyperparathyroidism hormones and electrolytes imbalance
↑PTH = Hypercalcemia, Hypophosphatemia
97
Primary Hyperparathyroidism is a________ disease
and there is
and
Sporadic
Excess production PTH by one or more PT glands
Loss of feedback control
98
Primary Hyperparathyroidism % adenoma and hyperplasia
• 85% PT adenoma, 15% PT hyperplasia
99
In Primary Hyperparathyroidism what happens to phos -->
• ↓Phos due to ↑ ↑ ↑ urinary excretion of Phosphate• Increased Phosphate depletion impairs tubular
reabsorption of Bicarbonate = Metabolic Acidosis
100
Secondary Hyperparathyroidism : electrolyte Ca and phos
Secondary ↓Ca, ↑Phos
101
Secondary Hyperparathyroidism is
↑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
• Other causes of Secondary Hyperparathyroidism
Phenytoin, phenobarbital,
laxatives – accelerate Vit. D catabolism or
decrease intestinal absorption of Ca.
103
Tertiary Hyperparathyroidism electrolyte imbalance
| •
↑Ca
104
Tertiary Hyperparathyroidism
* Occurs following long-standing Secondary HPT
| * Subsequently results later in Hypercalcemia
105
Etiology of Tertiary Hyperparathyroidism ? What does it present with? Normally PT tissues is not
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
HYPOPARATHYROIDISM: Phos and Ca
↓Ca, ↑Phos
107
Hypoparathyroidism there is ______ caused by
↓PTH
• Caused by damage to PT gland during thyroid
surgery
108
Explain the electrolyte imbalance with hypoparathyroidism
• Hypocalcemia
• Hyperphosphatemia due to loss of PTH effects
at kidney. (Normally PTH↑ urinary excretion of Phosphate).
109
Hypoparathyrodism: Hyper and hypopara
↓Ca, ↑Phos like secondary hyperpara, but
| without renal failure = hypopara
110
Hypocalcemia lowers
• Lowers threshold for nerve and muscle
excitation. Even slight stimulus can initiate
nerve impulse.
111
Hypocalcemia Creates Tetany:
```
– Muscle spasms
– Hyperreflexia
– Tonic-clonic convulsions
– Laryngeal spasms
– Death from asphyxiation
```
112
Hypocalcemia signs
• Chvostek and Trousseau signs evaluate
| neuromuscular irritability
113
Treat hypocalcemia Treat with
• Treatment: calcium and Vit. D
114
Most popular technique for thyroid surgery is
General anesthesia.
115
Regional anesthesia possible with cervical plexus block, but carries risks (4)
– Vocal cord dysfunction from block
– Damage to vertebral artery
– Damge to phrenic nerve
– Damage to S.C.
116
Anesthesia Considerations - Airway
| Goiters may cause (4)
– Tracheal deviation
– Distortion of laryngeal inlet
– Erosion Erosion of tracheal rings of tracheal rings
– post -op airway collapse
117
What do you do on Extubation for Thyroid?
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
Thyroid disorder: Anesthesia Considerations - Positioning.
| Airway
Once airway secured, pt. usually positioned with
padding under shoulders; and neck extended on
a head ring
119
Thyroid disorder: Anesthesia Considerations - Positioning.
| • Sterile draping generally includes
split towel wrapped around the head, this will require
| disconnect from anesthesia circuit and subsequent positioning of the pt.
120
Thyroid disorder: Anesthesia Considerations - Positioning: Movement
Movement can cause endotracheal tube to become displaced. Its proper positioning must be rechecked before surgery commences.
121
Regional anesthesia possible with cervical plexus block, but carries risks (4)
– Vocal cord dysfunction from block
– Damage to vertebral artery
– Damge to phrenic nerve
– Damage to S.C.
122
Anesthesia Considerations - Airway
| Goiters may cause (4)
– Tracheal deviation
– Distortion of laryngeal inlet
– Erosion Erosion of tracheal rings of tracheal rings
– post -op airway collapse
123
What do you do on Extubation for Thyroid?
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
Thyroid disorder: Anesthesia Considerations - Positioning.
| Airway
• Once airway secured, pt. usually positioned with
padding under shoulders; and neck extended on
a head ring
125
Thyroid disorder: Anesthesia Considerations - Positioning.
| • Sterile draping generally includes
split towel wrapped around the head, this will require
| disconnect from anesthesia circuit and subsequent positioning of the pt.
126
Thyroid disorder: Anesthesia Considerations - Positioning: Movement
Movement can cause endotracheal tube to become displaced. Its proper positioning must be rechecked before surgery commences.
127
Why does hyperthyroidism medications takes a long time to take effect?
Destroys glands over time not overnight
| Slow death of gland
128
Pt has breast cancer, uncontrolled amounts of parathyroid hormone related peptide. Why are they drawing blood for calcium
Tooo high because cancer cells are causing increase production.
129
HOw can little gland in neck makes my bones weak.
CAlcium regulation, increase blood calcium, decrease bone CA make then weak and they break
130
Blowing BP cuff and looking at hand
Checking trousseau sign to screen for low CA, (carpopedal spasm)
131
Why labs check for level of proteins?
Thyroid + steroid need transport proteins hormones
132
Most likely to happen with body weight and tolerance of heat and cold when the gland is destroyed
Hypothyroidism
| Weight gain and cold intolerance.
133
Hypothyroidism on P wave and QRS
```
Decrease p wave
Decrease QRS complex
Increase QT
Torsade
Bradycardia
```
134
Hyperthyroidism on CV
Tachy
Increase rate and output
Cardiomyopathy
135
Why does people with hyperparathyroidism are predisposed to form kidney stones
Increase blood Ca levels
| Increase resorption of Ca in DCT
136
What is the difference between Thyrotoxicosis and Thyrotoxic crisis?
Thyrotoxicosis -> Hyperthyroidism
| Thyrotoxic crisis--> Thyroid storm (death within 48 hrs, undiagnosed
137
When tumor destroys thyroid gland what happens to thyroid glands, blood lvels of TRH
TSH
| and TRH goes up
138
↓TH leads to
↑TSH – could cause goiter.
139
• Treatment with iodine replacement. If goiter is
| present
additional treatment
140
Hyperparathyroidism Signs and symptoms
Fatigue, HA, Depressio, Anorexia, NV, CV disease, HTN , pathologic fractures
141
Hypoparathyroidism Signs and symptoms
Tetany, Chovesk sign (face),. Trousseau, (arm) Tracheal deviation, distortion of laryngeal inlet, erosion of tracheal rings.
142
Enlargement of the thyroid gland is called a _____and is a response to increased stimulation by
Goiter ; TSI (overstimulation of TSH)
143
Cretinism is caused by untreated
Congenital Hyperthyroidism
144
Calcitonin is secreated by the _________and help regulate plasma ____concentration
Thyroid glands ; Calcium
145
Role of beta blockers in the treatment of Hyperthyrodism
Propranolol
Inhibits T4 conversion to T3
sympathetic tachycardia and nausea
146
What are the neuromuscular signs and symptoms of hyperparathyroidism
Increase Ca may antagonize, NDNMBA continue monitoring
